Effect of cooling on vascular smooth muscle from the thirteen-lined ground squirrel

Peripheral vascular resistance in the ground squirrel (Spermophilus tridecemlineatus) increases when the animal enters hibernation. The goals of this study were to determine if a change in vascular reactivity contributes to this hemodynamic response, and to compare the effects of temperature on vascular responsiveness in a hibernator (ground squirrel) and a nonhibernating mammal (rat). Helically cut strips of aortae and femoral arteries were mounted in organ chambers (37 degrees C) and isometric contractions were recorded. The arteries were made to contract in response to exogenous norepinephrine (5.9 X 10(-7) M). Cooling the organ chamber (11 degrees C) potentiated contractions to norepinephrine (5-15% increase) in ground squirrel femoral arteries but depressed those (80-100% decrease) in ground squirrel aortae and rat aortae and femoral arteries. Contractions in response to depolarizing concentrations of potassium in ground squirrel femoral arteries were depressed by cooling (11 degrees C), suggesting that the augmented response to norepinephrine at low temperature is specific. Treatment with indomethacin, propanolol, and ouabain did not alter the potentiating effect of temperature on contractions to norepinephrine in ground squirrel femoral arteries. Apparently, the potentiation is not related to prostaglandins generated in the vascular wall, to blockade of beta-adrenergic receptors, nor to inhibition of the electrogenic sodium pump. The observations are consistent with the hypothesis that a change in vascular responsiveness contributes to the regional control of blood flow in hibernation. This adaptive response is specific in that it does not occur in the aorta of the ground squirrel and the response is not present in the vasculature of the rat, a nonhibernating mammal.     

Distribution of the vasoconstrictor and vasorelaxant effects of norbormide along the vascular tree of the rat

Norbormide is a vasoconstrictor of rat peripheral arteries and a relaxant in rat aorta. To characterise norbormide actions within the rat vascular tree we have investigated its effects on the contractile function of rings from several arteries and veins. A maximal norbormide concentration (50 microM) failed to contract thoracic aorta and carotid artery, whereas in pulmonary artery, abdominal aorta, iliac, caudal, and femoral arteries it induced a contractile effect that was respectively 4.8 +/- 0.6, 18.4 +/- 1.5, 39 +/- 5, 144 +/- 7, and 260 +/- 22% of that induced by 90 mM KCl. In pulmonary, carotid, and iliac arteries, and in thoracic and abdominal aorta, 50 microM norbormide inhibited KCl-induced responses. Norbormide (50 microM) contracted all veins investigated. The effect, expressed as % of KCl-induced contraction, was 121 +/- 25, 154 +/- 14.5, 154 +/- 18.2, 203 +/- 19, and 267 +/- 33 for pulmonary vein, thoracic and abdominal vena cava, iliac and jugular veins, respectively. In jugular vein, as previously shown in rat caudal artery, norbormide contraction was abolished in Ca2+-free medium, was unaffected by the Ca2+ channel blocker nifedipine, and was relaxed by SK&F 96365, a blocker of store-operated Ca2+ channels. In conclusion: i) rat veins represent the main target for contractile norbormide action; ii) in both artery and veins norbormide contractions are generally inversely related to the calibre of the vessel; iii) norbormide-induced contraction is mediated by the same mechanism/s in arteries and veins; iiii) in norbormide-contracted arteries the drug activates both contractile and relaxing mechanisms.     

Comparison of Invasive Blood Pressure Measurements from the Caudal Ventral Artery and the Femoral Artery in Male Adult SD and Wistar Rats

Background and Purpose

Studies have suggested that the caudal ventral artery is a potential site for continuous arterial blood pressure monitoring in rats. However, the agreement of mean arterial pressure values between the femoral artery and the caudal ventral artery has not been investigated. This study was performed to identify whether the caudal ventral artery could be safely used for continuous blood pressure monitoring as an alternative site to the femoral artery.

Methods

Rats were randomized into four groups: Sprague Dawley rats under normothermia; Wistar rats under normothermia; Sprague Dawley rats under hypothermia; Wistar rats under hypothermia. Each rat underwent simultaneous monitoring of blood pressure using femoral artery and caudal ventral artery catheterization during a stable hemodynamic state and three periods of acute severe hemodynamic changes. The effects of rat strain, rectal temperature, experimental time course and hemodynamic factors on pressure gradients, the concordance of mean arterial pressure values between the femoral artery and the caudal ventral artery, and the rates of distal ischemia after surgery were determined.

Results

There was a significant difference in the rate of distal ischemia between femoral and caudal ventral arteries after catheterization (25% vs 5%, P<0.05). The overall mean gradient and the mean gradient under a steady hemodynamic state were 4.9±3.7 mm Hg and 5.5±2.5 mm Hg, respectively. The limits of agreement (bias±1.96 SD) were (−2.5 mm Hg, 12.3 mm Hg) and (-0.5 mm Hg, 10.5 mm Hg), respectively. Although the concordance decreased during the first 30 sec of each period of severe hemodynamic changes, the degree of agreement was acceptable regardless of the effects of rat strain and rectal temperature.

Conclusions

Based on the degree of agreement and the safety of catheterization, the caudal ventral artery may be a preferred site for continuous arterial blood pressure monitoring without acute severe hemodynamic changes.     

Functional assessment of human femoral arteries after cryopreservation

An established method for the cryopreservation of human femoral arteries for subsequent transplantation as allografts has been studied with particular attention to preservation of smooth muscle and endothelium. Human femoral arteries (HFAs) were harvested from multi-organ donors. Two groups were established; a control group of unfrozen HFAs and a group of cryopreserved HFAs. Cryopreservation was performed using RPMI solution containing dimethyl sulfoxide and the rate of cooling was 1 degrees C/min to -40 degrees C and faster thereafter until -150 degrees C was reached. The contraction and relaxation responses of unfrozen and frozen/thawed arteries were assessed by measurement of the isometric force generated by the HFAs in an organ bath. After thawing (warming was at 15 degrees C/min) the maximal contractile response to noradrenaline was 43% of the response of unfrozen HFAs. The endothelium-independent response to sodium nitroprusside was not altered, whereas the endothelium-dependent relaxation response to acetylcholine was slightly altered. The cryopreservation method used provided limited preservation of the contractility of human femoral arteries, and good preservation of both endothelium-independent and endothelium-dependent relaxation responses.     

Hypotension in the chronically hypoxic chicken embryo is related to the β-adrenergic response of chorioallantoic and femoral arteries and not to bradycardia

Prolonged fetal hypoxia leads to growth restriction and can cause detrimental prenatal and postnatal alterations. The embryonic chicken is a valuable model to study the effects of prenatal hypoxia, but little is known about its long-term effects on cardiovascular regulation. We hypothesized that chicken embryos incubated under chronic hypoxia would be hypotensive due to bradycardia and βAR-mediated relaxation of the systemic and/or the chorioallantoic (CA) arteries. We investigated heart rate, blood pressure, and plasma catecholamine levels in 19-day chicken embryos (total incubation 21 days) incubated from day 0 in normoxia or hypoxia (14-15% O(2)). Additionally, we studied α-adrenoceptor (αAR)-mediated contraction, relaxation to the β-adrenoceptor (βAR) agonist isoproterenol, and relaxation to the adenylate cyclase activator forskolin in systemic (femoral) and CA arteries (by wire myography). Arterial pressure showed a trend toward hypotension in embryos incubated under chronic hypoxic conditions compared with the controls (mean arterial pressure 3.19 ± 0.18 vs. 2.59 ± 0.13 kPa, normoxia vs. hypoxia, respectively. P = 0.056), without an accompanied bradycardia and elevation in plasma norepinephrine and lactate levels. All vessels relaxed in response to βAR stimulation with isoproterenol, but the CA arteries completely lacked an αAR response. Furthermore, hypoxia increased the sensitivity of femoral arteries (but not CA arteries) to isoproterenol. Hypoxia also increased the responsiveness of femoral arteries to forskolin. In conclusion, we suggest that hypotension in chronic hypoxic chicken embryos is the consequence of elevated levels of circulating catecholamines acting in vascular beds with exclusive (CA arteries) or exacerbated (femoral arteries) βAR-mediated relaxation, and not a consequence of bradycardia.     

Natural incidence of interruptions in the internal elastic lamina of caudal and renal arteries of the rat

Interruptions in the internal elastic lamina (IEL) have been quantified by light microscopy in the caudal arteries of different strains of rats and in caudal and renal arteries of (i) male and female virgin rats up until 2 years of age, (ii) repeatedly bred rats and (ii) hypertensive rats. Results showed that gaps in the IEL exist in caudal arteries of adult males in all strains studied, but to a lesser extent in the hairless mutant. In the virgin Wistar rat these interruptions in the IEL form with age in both caudal and renal arteries, and are more numerous (i) in the male than in the female in both arteries, and (ii) in the caudal than in the renal artery in both sexes. Repeated breeding in the Wistar rat abolishes the sex difference in incidence of IEL gaps in both renal and caudal arteries. The Sprague-Dawley breeder rat is more susceptible than the Wistar breeder to their formation in the renal artery. Hypertension in the male consistently increases the formation of IEL gaps in the renal but not in the caudal artery. The importance of local factors, e.g. hemodynamics, in the formation of these defects in the IEL, and their possible relationship with the development of arteriosclerosis is discussed.     

Development of fetal vascular responses to endothelin-1 and acetylcholine in the sheep

Responses to K(+), endothelin-1 (ET-1), and acetylcholine (ACh) of isolated adrenal, femoral, middle cerebral, and renal arteries from fetal [110--145 days gestational age (dGA, term approximately 148 dGA)] and 0- to 24-h newborn (NB) lambs were evaluated using the technique of wire myography. Responses at distinct developmental ages for each vascular bed were compared. In all arteries sensitivity to K(+)-induced vasoconstriction was similar at all fetal age points examined. In contrast, sensitivity to ET-1 increased with increasing fetal age in arteries from all vascular beds. The magnitude of the maximal vasoconstriction was positively correlated with GA for K(+) in adrenal, femoral, and cerebral arteries and for ET-1 in femoral, cerebral, and renal arteries. Cerebral arteries showed a greater sensitivity when compared with the other systemic arteries to K(+) and ET-1 at all fetal ages and to K(+) in NB. ACh evoked relaxatory responses in fetal and NB femoral and adrenal arteries. However, renal arteries relaxed comparatively less in response to ACh, and no vasodilation was noted in middle cerebral arteries at any age points examined. For femoral arteries ACh-induced vasorelaxation decreased with increasing GA but was restored in arteries from NB lambs. In summary, the responsiveness of isolated resistance arteries varies with developmental age in the fetal and perinatal sheep and these effects are both agonist and vascular bed specific. The augmented sensitivity in response to ET-1 of middle cerebral compared with other systemic arteries may reflect the importance of cerebral blood flow control during this critical developmental period.     

The ultrastructure of peripheral arteries during the development of DOCA hypertension in the rat

Summary The ultrastructure of the unconstricted superficial epigastric and femoral arteries is described in normal rats and in animals with hypertension induced by unilateral nephrectomy, by subcutaneous injections of desoxycorticosterone acetate and drinking of 1% NaCl. The femoral artery showed by far the greater response to the DOCA-saline treatment. In both vessels, the smooth-muscle cells changed from the normal spindle shape to a blunt ended outline with numerous pinocytotic vesicles and prolific collagen production. With long term hypertension, particularly in the femoral artery, the smooth-muscle cell profiles became very irregular. Hypertrophy of the organelles of the smooth-muscle cells was associated with an increase in the intercellular material which gradually changed from a mainly collagenous character to mainly vesicular. Lysosomal activity indicated cell disintegration. White blood cells adhere to the endothelium in hypertensive rats and there was an increase in subendothelial material. The number of intimal smooth-muscle cells increased noticeably in the femoral artery. In both arteries, the adventitial fibroblasts hypertrophied in hypertensive rats. In animals with an elevated blood pressure the morphological response was observed as early as 4 to 7 days after initiation of treatment.This work was supported by grants from the British Columbia Heart Foundation and the Medical Research Council of Canada.The authors are indebted to Miyoshi Nakashima for her invaluable assistance with these experiments.     

Endothelium-dependent and -independent relaxation in the forelimb and hindlimb vasculatures of swine

Limb differences in endothelial function exist between arm and leg vasculatures of humans. The current investigation tested the hypothesis that forelimb and hindlimb vasorelaxation are similar in the absence of limb differences in blood pressure. Conduit arteries (brachials/femorals) and second order arterioles were harvested from 22 miniature Yucatan swine. In vitro assessment of vasorelaxation was determined by administering increasing doses of bradykinin (BK), acetylcholine (ACh), and sodium nitroprusside (SNP). The role of the nitric oxide synthase (NOS) and cyclooxygenase (COX) pathways was assessed in conduit arteries but not resistance arterioles through L-NAME (300 microM) and INDO (5 microM) incubation, respectively. The relaxation responses to BK and ACh were similar in brachial and femoral arteries. SNP relaxation response was greater in the brachial compared to femoral arteries. There were also no significant differences in the relaxation responses of second order arterioles of the forelimb and hindlimb to BK, ACh, and SNP. Incubation of conduit arterial rings in L-NAME produced a greater reduction in BK and ACh relaxation in the brachial (approximately 25%) compared to femoral (approximately 13%) arterial rings. The current results of this investigation suggest that the forelimb and hindlimb vasculatures of swine have relatively similar vasorelaxation responses to both endothelium-dependent and -independent vasodilators.     

Arterial vascularization of the tail of the pancreas with special reference to the relation of the tail and body vessels

The cauda pancreatis has a characteristic pattern of vascularization. Among the big arterial stems surrounding it, up to 4 arteries, 'caudal arteries', nourish the arterial system of the cauda. These stems originate especially in the Arteria gastroepiploica sinistra and in the lower main splenic branch of the Arteria lienalis. The vascular relations between corpus and cauda can be of different kinds. Five basic types of relations can be identified: type I: the cauda is supplied exclusively by caudal arteries; type II: at least one caudal artery anastomoses with the vessels of the corpus; type III: the cauda is supplied both by the caudal arteries and by vessels of the corpus (non-anastomosing); type IV: combined forms of blood supply by caudal arteries and corpus arteries by way of anastomoses and non-anastomosing vessels are found; type V: the cauda is supplied exclusively be vessels stemming from the corpus. In each of these five types, individual vessels supplying the cauda can assume the function of a terminal vessel.     

Selective accumulations of aluminum in five human arteries

The aim of the present study was to determine variability of aluminum (Al) accumulation in human arteries and to observe the relationship between Al and five other elements (Ca, Fe, Mg, P, and Si) in the arteries. The Al contents in the thoracic aorta, basilar, coronary, femoral, and radial arteries of 26 human subjects were estimated by an inductively coupled plasma-atomic emission spectrometer and compared quantitatively to five elements. Al was detected in 88% of the cases in both the femoral and radial arteries, 73% in the coronary artery, 58% in the aorta, and 31% in the basilar artery. The average Al content was highest in the femoral artery (48.3 ± 15.0 μg/g dry weight) and lowest in the basilar artery (8.1 ± 3.6 μg/g). The Al had positive correlations with P, Ca, or Mg in both the aorta and femoral artery, and with Ca or P in the basilar artery. In the coronary artery, a correlation was found between Al and Si. No relationships were found between Al and each of the five elements in the radial artery. From these results, Al varied widely among the five arteries and accumulated more in the femoral and radial arteries but less in the basilar artery. These accumulations of Al were positively correlated with Ca or P in several arteries, but not sufficiently to explain the accumulation of Al. Further investigations are required to understand the mechanism of the variability of Al accumulation in the arteries.     

Endothelium-dependent and -independent vasodilation of the superficial femoral artery in spinal cord-injured subjects

Extreme inactivity of the legs in spinal cord-injured (SCI) individuals does not result in an impairment of the superficial femoral artery flow-mediated dilation (FMD). To gain insight into the underlying mechanism, the present study examined nitric oxide (NO) responsiveness of vascular smooth muscles in controls and SCI subjects. In eight healthy men (34 +/- 13 yr) and six SCI subjects (37 +/- 10 yr), superficial femoral artery FMD response was assessed by echo Doppler. Subsequently, infusion of incremental dosages of sodium nitroprusside (SNP) was used to assess NO responsiveness. Peak diameter was examined on a second day after 13 min of arterial occlusion in combination with sublingual administration of nitroglycerine. Resting and peak superficial femoral artery diameter in SCI subjects were smaller than in controls (P < 0.001). The FMD response in controls (4.2 +/- 0.9%) was lower than in SCI subjects (8.2 +/- 0.9%, P < 0.001), but not after correcting for area under the curve for shear rate (P = 0.35). When expressed as relative change from baseline, SCI subjects demonstrate a significantly larger diameter increase compared with controls at each dose of SNP. However, when expressed as a relative increase within the range of diameter changes [baseline (0%) - peak diameter (100%)], both groups demonstrate similar changes in response to SNP. Changes in diameter during SNP infusion and FMD response are larger in SCI subjects compared with controls. When these results are corrected, superficial femoral artery FMD and NO sensitivity in SCI subjects are not different from those in controls. This illustrates the importance of appropriate data presentation and suggests that, subsequent to structural inward remodeling of conduit arteries as a consequence of extreme physical inactivity, arterial function is normalized.     

Sympathetic innervation promotes vascular smooth muscle differentiation

The sympathetic nervous system (SNS) is an important modulator of vascular smooth muscle (VSM) growth and function. Several lines of evidence suggest that the SNS also promotes VSM differentiation. The present study tests this hypothesis. Expression of smooth muscle myosin (SM2) and alpha-actin were assessed by Western analysis as indexes of VSM differentiation. SM2 expression (normalized to alpha-actin) in adult innervated rat femoral and tail arteries was 479 +/- 115% of that in noninnervated carotid arteries. Expression of alpha-actin (normalized to GAPDH or total protein) in 30-day-innervated rat femoral arteries was greater than in corresponding noninnervated femoral arteries from guanethidine-sympathectomized rats. SM2 expression (normalized to alpha-actin) in neonatal femoral arteries grown in vitro for 7 days in the presence of sympathetic ganglia was greater than SM2 expression in corresponding arteries grown in the absence of sympathetic ganglia. In VSM-endothelial cell cultures grown in the presence of dissociated sympathetic neurons, alpha-actin (normalized to GAPDH) was 300 +/- 66% of that in corresponding cultures grown in the absence of neurons. This effect was inhibited by an antibody that neutralized the activity of transforming growth factor-beta2. All of these data indicate that sympathetic innervation increased VSM contractile protein expression and thereby suggest that the SNS promotes and/or maintains VSM differentiation.     

Exercise training improves femoral artery blood flow responses to endothelium-dependent dilators in hypercholesterolemic pigs

We tested two hypotheses: 1) that the effects of hypercholesterolemia on endothelial function in femoral arteries exceed those reported in brachial arteries and 2) that exercise (Ex) training enhances endothelium-dependent dilation and improves femoral artery blood flow (FABF) in hypercholesterolemic pigs. Adult male pigs were fed a normal fat (NF) or high-fat/cholesterol (HF) diet for 20 wk. Four weeks after the diet was initiated, pigs were Ex trained or remained sedentary (Sed) for 16 wk, thus yielding four groups: NF-Sed, NF-Ex, HF-Sed, and HF-Ex. Endothelium-dependent vasodilator responses were assessed in vivo by measuring changes in FABF after intra-arterial injections of ADP and bradykinin (BK). Endothelium-dependent and -independent relaxation was assessed in vitro by measuring relaxation responses to BK and sodium nitroprusside (SNP). FABF increased in response to ADP and BK in all groups. FABF responses to ADP and BK were not impaired by HF but were improved by Ex in HF pigs. BK- and SNP-induced relaxation of femoral artery rings was not altered by HF or Ex. To determine whether the mechanism(s) for vasorelaxation of femoral arteries was altered by HF or Ex, BK-induced relaxation was assessed in vitro in the absence or presence of N(G)-nitro-l-arginine methyl ester [l-NAME; to inhibit nitric oxide synthase (NOS)], indomethacin (Indo; to inhibit cyclooxygenase), or l-NAME + Indo. BK-induced relaxation was inhibited by l-NAME and l-NAME + Indo in all groups of femoral arteries. Ex increased the NOS-dependent component of endothelium-dependent relaxation in NF (not HF) arteries. Indo did not inhibit BK-induced relaxation. Collectively, these results indicate that hypercholesterolemia does not alter endothelial function in femoral arteries and that Ex training improves FABF responses to ADP and BK; however, the improvement cannot be attributed to enhanced endothelial function in HF femoral arteries. These data suggest that Ex-induced improvements in FABF in HF arteries are mediated by vascular adaptations in arteries/arterioles downstream from the femoral artery.     

Inhibitory effects of L-NG-nitro-arginine on the synthesis of EDRF and the cerebroarterial response to vasodilator nerve stimulation

Treatment with L-NG-nitro-arginine (L-NA) inhibited the brady-kinin-induced relaxation, mediated via EDRF, in dog coronary artery strips partially contracted with prostaglandin F2 alpha; the inhibition was prevented by L-, but not D-, arginine. Relaxation caused by nitroglycerin was not altered by L-NA. The release of EDRF, as assayed using dog coronary artery strips without endothelium, from perfused femoral artery segments with endothelium in response to acetylcholine and substance P was significantly reduced by treatment of the femoral artery with L-NA. The inhibitory effect was reversed by L-arginine. Relaxant responses of dog cerebral artery strips with and without endothelium to electrical stimulation of non-adrenergic, non-cholinergic nerves were suppressed by L-NA, whereas relaxation of coronary arteries with and without endothelium by the stimulation of adrenergic nerves was not influenced. The L-NA-induced inhibition was reversed by L-arginine. It is speculated that L-NA inhibits the synthesis of EDRF, as does L-NG-monomethyl arginine, and NO-like substance(s) produced plays an important role in transferring information from vasodilator nerves to smooth muscle in cerebral arteries.     

Contractile and relaxant responses of diabetic dog femoral arteries

Strips of femoral arteries of normal and alloxan-treated dogs were set up for isometric recording. The contractile response to phenylephrine and the relaxant response to acetylcholine were determined. Neither alloxan treatment nor mechanical removal of endothelium altered the EC50 value for phenylephrine. The slope of phenylephrine dose-response curves of diabetic and healthy vessels with intact endothelium was similar, whereas the slope of phenylephrine dose-response curves of endothelium-denuded diabetic arteries was significantly greater than that of the denuded healthy arteries. Removal of the endothelium completely abolished the relaxant effect of acetylcholine. The relaxant potency (IC50) of acetylcholine was not affected by alloxan treatment. The results suggest that in canine femoral arteries the relaxant activity of acetylcholine is unaffected in experimental diabetes and the damage of the arterial endothelium may play a role in the increased responsiveness of diabetic vessels to adrenergic agonists.     

Analysis of the contraction induced by isoproterenol in isolated cerebral and femoral arteries of cat

The vasoconstrictor responses induced by isoproterenol in cylindrical segments of posterior communicating and femoral arteries of the cat were analyzed. For this purpose, dose-response curves for isoproterenol before and after addition of propranolol (5 X 10(-9) to 10(-6) M) or phentolamine (10(-6) M) to the bath were determined. Propranolol did not significantly change the contraction induced by isoproterenol in cerebral and femoral arteries. Phentolamine reduced the contractile responses of cerebral arteries evoked by all concentrations of isoproterenol. However phentolamine shifted the dose-response curve to isoproterenol in femoral arteries to the right, the pA2 value for this antagonist being 6.74. These results indicate that the alfa adrenoceptors are involved in the contraction caused by isoproterenol in femoral arteries, whereas in brain arteries other receptors or mechanisms are also likely involved.     

Response of Various Conduit Arteries in Tachycardia- and Volume Overload-Induced Heart Failure

Although hemodynamics changes occur in heart failure (HF) and generally influence vascular function, it is not clear whether various HF models will affect the conduit vessels differentially or whether local hemodynamic forces or systemic factors are more important determinants of vascular response in HF. Here, we studied the hemodynamic changes in tachycardia or volume-overload HF swine model (created by either high rate pacing or distal abdominal aortic-vena cava fistula, respectively) on carotid, femoral, and renal arteries function and molecular expression. The ejection fraction was reduced by 50% or 30% in tachycardia or volume-overload model in four weeks, respectively. The LV end diastolic volume was increased from 65±22 to 115±78 ml in tachycardia and 67±19 to 148±68 ml in volume-overload model. Flow reversal was observed in diastolic phase in carotid artery of both models and femoral artery in volume-overload model. The endothelial function was also significantly impaired in carotid and renal arteries of tachycardia and volume-overload animals. The endothelial dysfunction was observed in femoral artery of volume-overload animals but not tachycardia animals. The adrenergic receptor-dependent contractility decreased in carotid and femoral arteries of tachycardia animals. The protein expressions of NADPH oxidase subunits increased in the three arteries and both animal models while expression of MnSOD decreased in carotid artery of tachycardia and volume-overload model. In conclusion, different HF models lead to variable arterial hemodynamic changes but similar vascular and molecular expression changes that reflect the role of both local hemodynamics as well as systemic changes in HF.     

Heterogeneity in responses of isolated monkey arteries and veins to atrial natriuretic peptide

Regional differences in responses of isolated monkey arteries and veins to atrial natriuretic peptide were investigated by recording isometric tension. Addition of atrial natriuretic peptide (4 X 10(-12) to 4 X 10(-8) M) produced a concentration-dependent relaxation in isolated monkey arteries and veins. No significant difference was observed between the responses to rat and human atrial natriuretic peptides. A marked heterogeneity in responses to rat atrial natriuretic peptide, however, was observed in arterial preparations. The decreasing order of the response was as follows: renal greater than pulmonary greater than femoral = mesenteric greater than coronary greater than middle cerebral greater than basilar arteries. A heterogeneity in the relaxation produced by atrial natriuretic peptide was also observed in monkey veins. The decreasing order of the response was as follows: pulmonary greater than mesenteric = portal greater than femoral greater than renal = inferior caval veins. On the other hand, 10(-5) M sodium nitroprusside caused a maximal relaxation in all monkey arteries and veins used. In the middle cerebral, basilar, and coronary arteries, the relaxant effects of rat atrial natriuretic peptide on KCl-induced contraction were significantly smaller than those on the preparations contracted by an agonist such as prostaglandin F2 alpha. These results suggest that there exist profound regional vasorelaxant selectivities of atrial natriuretic peptide in isolated monkey arteries and veins.     

Endothelium-dependent relaxation differs in porcine pulmonary arteries from the left and right caudal lobes.

We hypothesized that pulmonary arteries (PA) from identical branch orders within left and right caudal lung lobes would exhibit similar vasomotor responses. Arterial rings from caudal lung lobes of female swine were examined in vitro. Vascular smooth muscle contraction to KCl and norepinephrine did not differ. Vascular relaxation to endothelium-dependent (bradykinin, acetylcholine, A-23187) and -independent (sodium nitroprusside, zero-calcium Krebs solution) vasodilators was assessed. Right PA exhibited less maximal relaxation to acetylcholine (50%) than did left PA (69%; P < 0.001). Maximal relaxation to sodium nitroprusside did not differ, although right PA had a lower drug concentration resulting in half-maximal relaxation (6.26 x 10(-8) M) than did left PA (9.57 x 10(-8) M; P < 0.05). Nitric oxide synthase inhibition with an arginine analog (N(omega)-nitro-L-arginine methyl ester) depressed acetylcholine-induced relaxation but the left vs. right difference persisted. Indomethacin enhanced relaxation to acetylcholine and abolished the difference between left and right. We conclude that endothelium-dependent vasorelaxation is less in porcine right than in left PA because of greater release of one or more constricting prostanoids in arteries from the right caudal lobe.