Reflex pressure response to the electric stimulation of different parts of the rat stomach

The role of the autonomic nervous system in the pressor response to the electrical stimulation of different gastric zones has been studied in rats. The stimulus was applied before and after the following interventions: bilateral vagotomy, ganglionic blockade, alpha-adrenergic receptor blockade and beta-adrenergic receptor blockade. After the ganglionic blockade no pressor responses to the electrical stimulus were observed. After the alpha-adrenergic blockade a lower pressor response was observed. A hypertensive response can be induced by mechanical, chemical or electrical stimulation of gastric receptors. It is concluded that the pressor reflex following the application of an electrical stimulus on different zones of the digestive tract is mediated by the sympathetic nervous system and that the efferent pathways are mainly alpha-adrenergic ones.     

Alpha-adrenergic tone in the coronary circulation of the conscious dog

To examine the role of neural factors in the control of coronary vasoactivity in conscious animals, dogs were supplied with miniature pressure gauges in the aorta and left ventricle (to measure aortic and left ventricular pressures, respectively and with a flow probe on the left circumflex coronary artery (to measure coronary blood flow). The experiments were conducted several weeks after recovery from operation. Stimulation of the carotid chemoreceptor and pulmonary inflation elicited a biphasic reflex response. Initially, coronary vasodilation was observed; coronary blood flow tripled even after changes in metabolic factors were minimized by pretreatment with propranolol. A similar response occurred after a spontaneous deep breath. The coronary vasodilation could be blocked by alpha-adrenergic receptor blockade. The second phase of the response involved an increase in coronary vascular resistance, associated with elevated arterial pressure and an absolute reduction in coronary blood flow and coronary sinus oxygen content. The secondary coronary vasoconstriction was also abolished by alpha-adrenergic blockade. Paradoxically, alpha-adrenergic receptor blockade with phentolamine (at constant heart rate and after beta-adrenergic receptor blockade) did not increase coronary blood flow and reduced coronary vascular resistance only slightly. Selective alpha 1-adrenergic receptor blockade with prazosin and trimazosin on different days induced progressively greater reductions in coronary vascular resistance. Trimazosin was the only alpha-adrenergic receptor blocker to elevate coronary blood flow significantly. It is conceivable, but speculative, that withdrawal of alpha-adrenergic tone may involve activation of an intermediate agent, which is a potent coronary vasodilator. Alternatively, withdrawal of alpha-adrenergic tone may be an important mechanism for immediate control of the coronary circulation, but under more chronic conditions it plays a lesser role as a result of suppression by metabolic factors.     

刺激大鼠蓝斑核区对胃电和胃运动的影响

用乌拉坦麻醉的大鼠,同步描记血压、胃电和胃运动,观察了刺激蓝斑核区对胃电和胃运动的影响,分析了其作用途径。实验结果表明,刺激蓝斑核区后血压平均升高60.5mmHg(P<0.001);胃电慢波的振幅由对照的0.52mV 减弱到0.18mV(P<0.001)。快波的振幅和频率也减少。胃内压平均下降到对照值的29.9％(P<0.001)。在横断颈髓的动物刺激蓝斑核区后血压的升高幅度明显减弱,平均升高9mmHg,升压效应的潜伏期明显延长;胃电慢波的振幅由对照的0.53mV 减弱到 0.24mV(P<0.001)。胃内压平均下降到对照值的45.1％。对胃电和胃运动的这种抑制效应可被切断迷走神经所完全消除。在事先切断迷走神经但脊髓仍保留完整的动物,刺激蓝斑核区使胃内压平均下降36.6％(P<0.01)。根据以上结果认为,蓝斑核区可能参与对胃电和胃运动的中枢性调节。此调节机制可能经由脊髓和迷走两条通路实现。     

Alpha-adrenergic stimulation of sarcolemmal protein phosphorylation and slow responses in intact myocardium

The effects of alpha- and beta-adrenergic stimulation on sarcolemmal protein phosphorylation and contractile slow responses were studied in intact myocardium. Isolated rat ventricles were perfused via the coronary arteries with 32Pi after which membrane vesicles partially enriched in sarcolemma were isolated from individual hearts. Alterations in the sarcolemmal slow inward Ca2+ current were assessed in the 32P-perfused hearts using a contractile slow response model. In this model, Na+ channels were first inactivated by partial depolarization of the hearts in 25 mM K+ after which alterations in Ca2+ channel activity produced by either alpha- or beta-adrenergic agonists could be assessed as restoration of contractions. alpha-Adrenergic stimulation (phenylephrine + propranolol) of the perfused hearts resulted in increased 32P incorporation into a 15-kDa sarcolemmal protein. This protein co-migrated with the 15-kDa sarcolemmal protein phosphorylated in hearts exposed to beta-adrenergic stimulation produced by isoproterenol. beta-Adrenergic stimulation, but not alpha-adrenergic stimulation, also resulted in phosphorylation of the sarcoplasmic reticulum protein, phospholamban. Phosphorylation of the 15-kDa protein in perfused hearts in response to either alpha- or beta-adrenergic stimulation was associated with restoration of contractions, indicative of increases in the slow inward Ca2+ current. Increases in 32P incorporation into the 15-kDa protein preceded restoration of contractions by phenylephrine. Nifedipine abolished the contractile responses to alpha-adrenergic stimulation while having no effect on increases in 15-kDa protein phosphorylation. The effects of alpha-adrenergic stimulation occurred in the absence of increases in cAMP levels. These results suggest that phosphorylation of the 15-kDa protein may be involved in increases in the slow inward current produced by stimulation of either alpha- or beta-adrenergic receptors.     

Adrenomedullary pressor responses to stimulation of the rostral hypothalamus in the rat: influence of adrenaline-induced vasodilation and reflex cardioinhibition

Electrical stimulation (100 Hz, 1 ms, 150 microA, 10 s) of the anterior hypothalamus in chloralose-anesthetized rats evoked a biphasic pressor response consisting of an initial sharp rise in arterial pressure at the onset of stimulation, followed by a second elevation after cessation of the stimulus. This response was accompanied by an increase in plasma noradrenaline and adrenaline levels. Peripheral sympathectomy with guanethidine selectively abolished the primary phase of the biphasic pressor response, while bilateral removal of the adrenal medulla eliminated only the secondary component. After alpha-adrenergic blockade with phentolamine, the primary phase of the stimulation-induced response was reduced while the secondary pressor component was blocked and replaced by a significant hypotension. The intravenous administration of sotalol enhanced the secondary pressor component without affecting the stimulation-induced plasma noradrenaline and adrenaline responses. After treatment with atropine, the secondary pressor effect was also potentiated, as the reflex bradycardia normally associated with the response was eliminated. A subsequent administration of sotalol in these rats further potentiated the secondary pressor component to stimulation. In rats treated with atropine and sotalol, the sympathetic vasomotor and the adrenomedullary pressor responses could be dissociated according to thresholds and stimulus frequency or current-response characteristics. The results suggest that in intact rats, adrenaline-induced vasodilation and reflex cardiac inhibition contribute to either reduce or mask the adrenomedullary component of the biphasic pressor response evoked by stimulation of the anterior hypothalamus. The study also raises the hypothesis of a dual regulation of both components of the sympathetic system in the anterior hypothalamic region.     

Effects of gastric distension on the cardiovascular system in rainbow trout (Oncorhynchus mykiss)

When animals feed, blood flow to the gastrointestinal tract increases to ensure an adequate oxygen supply to the gastrointestinal tissue and an effective absorption of nutrients. In mammals, this increase depends on the chemical properties of the food, as well as, to some extent, on the mechanical distension of the stomach wall. By using an inflatable nitrile balloon positioned in the stomach, we investigated the cardiovascular responses to mechanical stretch of the stomach wall in rainbow trout (Oncorhynchus mykiss). Distension with a volume equivalent to a meal of 2% of the body mass increased dorsal aortic blood pressure by up to 29%, and central venous blood pressure increased transiently nearly fivefold. The increase in arterial pressure was mediated by an increased vascular resistance of both the systemic and the intestinal circulation. Cardiac output, heart rate, and stroke volume (SV) did not change, and only transient changes in gut blood flow were observed. The increase in arterial pressure was abolished by the alpha-adrenergic antagonist prazosin, indicating an active adrenergic vasoconstriction, whereas the venous pressor response could be the consequence of a passive increase in intraperitoneal pressure. Our results show that mechanical distension of the stomach causes an instantaneous increase in general vascular resistance, which may facilitate a redistribution of blood to the gastrointestinal tract when chemical stimuli from a meal induce vasodilation in the gut circulation. The normal postprandial increase in gut blood flow in teleosts is, therefore, most likely partly dependent on mechanical stimuli, as well as on chemical stimuli.     

Comparative effect of atropine on the adrenergic and muscarinic stimulation of phospholipid 32P labelling in isolated parotid cells: atropine, a possible blocker of alpha-adrenergic receptors

The inhibitory effect of atropine on phospholipid 32P labelling stimulated by muscarinic or alpha-adrenergic agonists was studied in isolated parotid cells. Atropine (10(-11) to 10(-4) M) had no effect on phospholipid 32P labelling in unstimulated cells. In contrast, 10(-8) to 10(-7) M atropine provoked a competitive inhibition of the cholinergic stimulation (i.e. this effect was completely wiped out at high agonist concentration). The atropine app. KD for the muscarinic receptor was 5 X 10(-9) M. Moreover, atropine inhibits the adrenergic stimulation of phospholipid 32P labelling by decreasing the efficacity and potency of the adrenergic agonists. The atropine app. KD for the alpha-adrenergic receptor can be estimated at 10(-5) M. This inhibition of alpha-adrenergic stimulation appears to be specific since atropine was without effect on the substance P or beta-adrenergic stimulation. At very low concentration (10(-10) - 10(-9) M) atropine seems to be a modulator (activator) of the muscarinic or adrenergic agonist-receptor complex. From the present data, it is suggested that atropine, besides its classical blocker effect at the muscarinic receptor, at high concentration is a specific alpha-adrenergic antagonist.     

Comparative effect of atropine on the adrenergic and muscarinic stimulation of phospholipid 32P labelling in isolated parotid cells: atropine,a possible blocker of alpha-adrenergic receptors

The inhibitory effect of atropine on phospholipid 32P labelling stimulated by muscarinic or alpha-adrenergic agonists was studied in isolated parotid cells. Atropine (10(-11) to 10(-4) M) had no effect on phospholipid 32P labelling in unstimulated cells. In contrast, 10(-8) to 10(-7) M atropine provoked a competitive inhibition of the cholinergic stimulation (i.e. this effect was completely wiped out at high agonist concentration). The atropine app. KD for the muscarinic receptor was 5 × 10(-9) M. Moreover, atropine inhibits the adrenergic stimulation of phospholipid 32P labelling by decreasing the efficacity and potency of the adrenergic agonists. The atropine app. KD for the alpha-adrenergic receptor can be estimated at 10(-5) M. This inhibition of alpha-adrenergic stimulation appears to be specific since atropine was without effect on the substance P or beta-adrenergic stimulation. At very low concentration (10(-10) — 10(-9) M) atropine seems to be a modulator (activator) of the muscarinic or adrenergic agonist-receptor complex. From the present data, it is suggested that atropine, besides its classical blocker effect at the muscarinic receptor, at high concentration is a specific alpha-adrenergic antagonist.     

Adrenergic interactions in uterus and vascular smooth muscle in rats in vivo

Simultaneous blood pressure and uterine responses to norepinephrine infusions were recorded in urethane-anesthetized, pentolinium-indomethacin treated rats in natural estrus under conditions in which no blockers or blockers of alpha 1-, alpha 2-, and beta-adrenergic receptors or of "reuptake" of norepinephrine were present. The contributions of alpha 1- and alpha 2-adrenergic receptors to the blood pressure response were similar during the initial portion of the response. At later times, however, alpha 1-adrenergic receptors were responsible for the major portion of the response. The tachyphylaxis of the pressor response that occurs during norepinephrine infusion could be prevented by preventing norepinephrine "reuptake" with imipramine. In the uterus, the initial small alpha-adrenergic contractile response (seen only at the lowest infusion rate) was quickly overwhelmed by a beta-adrenergic relaxing component. Administration of the beta-adrenergic receptor blocker, propranolol, during norepinephrine infusion caused similar increases in blood pressure in control, yohimbine-, and prazosin-treated rats. Uterine contractions, in contrast, were only significantly elevated during beta-adrenergic receptor blockade when yohimbine or imipramine had also been administered.     

Combined NO and PG inhibition augments alpha-adrenergic vasoconstriction in contracting human skeletal muscle

Sympathetic alpha-adrenergic vasoconstrictor responses are blunted in the vascular beds of contracting muscle (functional sympatholysis). We tested the hypothesis that combined inhibition of nitric oxide (NO) and prostaglandins (PGs) restores sympathetic vasoconstriction in contracting human muscle. We measured forearm blood flow via Doppler ultrasound and calculated the reduction in forearm vascular conductance in response to alpha-adrenergic receptor stimulation during rhythmic handgrip exercise (6.4 kg) and during a control nonexercise vasodilator condition (using intra-arterial adenosine) before and after combined local inhibition of NO synthase (NOS; via N(G)-nitro-L-arginine methyl ester) and cyclooxygenase (via ketorolac) in healthy men. Before combined inhibition of NO and PGs, the forearm vasoconstrictor responses to intra-arterial tyramine (which evoked endogenous noradrenaline release), phenylephrine (a selective alpha1-agonist), and clonidine (an alpha2-agonist) were significantly blunted during exercise compared with adenosine treatment. After combined inhibition of NO and PGs, the vasoconstrictor responses to all alpha-adrenergic receptor stimuli were augmented by approximately 10% in contracting muscle (P <0.05), whereas the responses to phenylephrine and clonidine were also augmented by approximately 10% during passive vasodilation in resting muscle (P <0.05). In six additional subjects, PG inhibition alone did not alter the vasoconstrictor responses in resting or contracting muscles. Thus in light of our previous findings, it appears that inhibition of either NO or PGs alone does not affect functional sympatholysis in healthy humans. However, the results from the present study indicate that combined inhibition of NO and PGs augments alpha-adrenergic vasoconstriction in contracting muscle but does not completely restore the vasoconstrictor responses compared with those observed during passive vasodilation in resting muscle.     

家兔延髓腹侧防御反应相关神经元

实验在25只乌拉坦(700m/kg)、氯醛糖(35mg/kg)麻醉,肌肉麻痹,人工呼吸的家兔上进行。第一组16只家兔中,单或双脉冲刺激下丘脑和中脑防御反应区,在延髓腹侧记录刺激所兴奋的单位。大部分单位分布于网状巨细胞核腹侧α部。52％的单位有自发放电活动。用阈下强度同时刺激下丘脑和中脑,97％单位有兴奋反应,提示家兔下丘脑和中脑防御反应区在延髓腹侧有聚合投射。第二组9只家兔中,在延髓腹表面单侧应用甘氨酸滤纸片或电凝损毁时,血压轻度下降,刺激下丘脑和中脑防御反应区引起的升压反应也部分被阻断。双侧应用甘氨酸或损毁,血压下降到脊动物水平,升压反应几乎完全被阻断。上述结果提示家兔延髓腹侧神经元在维持正常血压水平和在中继防御反应传出通路中起重要作用。     

刺激家兔腹部迷走神经外周端引起的降压作用

本文对电刺激家兔腹部的迷走神经外周端所引起的降压反应进行了研究。在121只家兔中的实验结果表明:电刺激腹部迷走神经外周端可引起动脉压、小肠和后肢的灌流压同时降低,而心率则无明显变化。这一降压反应发生时,小肠静脉血中的组织胺含量较刺激前明显升高,然后恢复;将小剂量的组织胺 H_1受体阻断剂扑尔敏、非乃根和 H_2受体阻断剂甲氰咪胍(Cimetidine)分别注入肠系膜上动脉均能减弱刺激腹部迷走神经外周端引起的动脉压和小肠灌流压的降低。心得安能削弱此降压反应,而阿托品无效;切断两侧内脏大神经能显著削弱刺激腹部迷走神经外周端引起的降压反应。此残余的降压反应在注入抗组织胺剂后完全消失。由此推论,刺激家兔腹部迷走神经外周端引起的降压反应是通过中枢和外周两方面因素的作用,使血管舒张,外周阻力降低而实现的。     

Cardiovascular regulation during hypoxia in embryos of the domestic chicken Gallus gallus

Renewed interest in the use of the embryonic chicken as a model of perinatal cardiovascular regulation has inspired new questions about the control mechanisms that respond to acute perturbations, such as hypoxia. The objectives of this study were to determine the cardiovascular responses, the regulatory mechanisms involved in those cardiovascular responses, and whether those mechanisms involved the central nervous system (CNS) of embryonic chickens. Heart rate (f(H)) and blood pressure were measured in chicken embryos of different incubation ages during exposure to different levels of hypoxia (15, 10, and 5% O(2)). At all levels of hypoxia and at all developmental ages, a depression of f(H) and arterial pressure was observed, with the exception of day 20 embryos in 15 and 10% O(2). The intensity of the embryonic f(H) and blood pressure responses were directly related to the level of hypoxia used. Muscarinic and alpha-adrenergic receptor stimulation limited the hypoxic hypotension on days 15-19 and 15-21, respectively, as indicated after blockade with atropine and phentolamine. During the final 3 days of incubation, the intensity of the hypoxic hypotension was magnified due to alpha-vasodilation caused by beta-adrenergic and muscarinic receptor stimulation. In 19- to 21-day-old embryos, the f(H) response to hypoxia was limited by alpha-adrenergic receptor stimulation as indicated by the accentuated bradycardia after blockade with phentolamine. Furthermore, on day 21, atropine limited the hypoxic bradycardia, indicating that muscarinic receptors also play a role in the f(H) response at this age. In addition, the muscarinic actions on the heart and the adrenergic effects on the vasculature appeared to occur through a hypoxic-induced direct release from chromaffin tissue and autonomic nerve terminals. Thus, in embryonic chickens, the only cardiovascular response to hypoxia that involves the CNS was the cholinergic regulation of arterial pressure after day 15 of incubation. Therefore, although embryonic chickens and fetal sheep, the standard models of perinatal cardiovascular physiology, respond to hypoxia with a similar redistribution of cardiac output, the underlying mechanisms differ between these species.     

大鼠侧脑室注射神经降压素对血压的作用

雄性Ｓｐｒａｇｕｅ－Ｄａｗｌｅｙ大鼠,用乌拉坦腹腔麻醉,在侧脑室注射神经降压素（ＮＴ）（１０,２０μｇ）可引起血压升高或降低,心率减慢,预先ｉｃｖ ａ１受体阻断剂哌唑嗪,可阻断ＮＴ的中枢升压反应,预先ｉｃｖ Ｍ受体阻断剂硫酸阿托品,可阻断ＮＴ的中枢降压反应,预先ｉｃｖ Ｈ１受体阻断剂扑尔敏或Ｈ２受体阻断剂甲氰咪胍,对ＮＴ的中枢心血管效应均无明显影响。实验结果表明：脑中ＮＴ升高可使血压升高或降低;在     

Cardiovascular function in anesthetized miniature swine.

Miniature swine anesthetized with pentobarbital were studied with respect to their cardiovascular function under control conditions and in response to catecholamines, baroreceptor inhibition, bilateral vagotomy and vagal nerve stimulation. Measurements included aortic pressure, heart rate, intraventricular pressure and its maximum rate of rise during contraction, carotid blood flow and resistance, femoral blood flow and resistance, and renal blood flow and resistance. The cardiovascular actions of norepinephrine, epiniphrine and isoproterenol were similar to those in other mammals, and the adrenergic receptor mechanisms also were susceptible to blockade with phentolamine or propranolol. Inhibition of the carotid baroreceptors was accompanied by elevation of aortic pressure, reflex bradycardia and increased femoral and renal resistances. Bileteral vagotomy was followed by hypertension, tachycardia and increased renal resistance. Changes in femoral resistance to these procedures differed between the two strains of miniature swine studied. Stimulation of the peripheral end of either vagus nerve was accompanied by bradycardia without hypotension.     

Local application of neurotensin to abdominal organs triggers cardiovascular reflexes in guinea pigs: possible mechanisms

Intraabdominal (IAB) injections or topical application of neurotensin (NT) to the serosal surface of the ileum or stomach evoked dose-dependent increases of blood pressure and of heart rate in anesthetized guinea pigs. These effects were markedly reduced by prior animal treatment with a ganglion blocker, alpha and beta adrenoceptor blockers, as well as by exposure of the abdominal organs to lidocaine, a local anesthetic. The blood pressure and heart rate responses to IAB injections or topical application of NT to the ileum or stomach were both inhibited by animal pretreatment with capsaicin. Cervical vagotomy or atropine pretreatment did not prevent or alter the cardiovascular responses to IAB injections of NT. These results suggest the presence in some organs and/or tissues of the abdominal cavity of sympathetic, capsaicin-sensitive sensory nerve fibers which, upon stimulation by NT, produce reflex increases of blood pressure and of heart rate.     

Motor effects of gastrin releasing peptide (GRP) and bombesin in the canine stomach and small intestine

Close intraarterial injections of synthetic porcine gastrin releasing peptide (GRP) or bombesin stimulated contractions in the stomach and inhibited ongoing contractile activity in the small intestine of anaesthetized dogs. Contractile activity of the circular muscle was recorded by serosal strain gauges and phasic activity when desired was elicited by local field stimulation or intraarterial motilin injections. In the stomach (corpus and antrum) following tetrodotoxin blockade of field-stimulated contractions, the contractile response to either peptide was not present, suggesting that stimulation of receptors on nerves initiated contractions in the stomach. Similarly, in the small intestine, the inhibitory response was eliminated by tetrodotoxin suggesting a neural receptor. Pre-treatment with reserpine did not alter the inhibitory response, either in the presence or absence of atropine, therefore, adrenergic inhibitory mechanisms did not appear to be involved. The concentration of bombesin producing 50% inhibition of field stimulation (ED50) was increased following treatment with the putative M1 muscarinic antagonist, pirenzipine suggesting activation of M1 cholinergic inhibitory receptors by bombesin. After blockade by atropine of field-stimulated contractions and the contractile response to intraarterial acetylcholine, the ED50 for bombesin inhibition of motilin contractions was increased. After muscarinic blockade, the residual inhibitory response of GRP/bombesin may involve activation of a neural non-cholinergic non-adrenergic inhibitory mechanism. These results suggest that GRP and bombesin act to alter motility in the dog in vivo by affecting neural activity.     

Inhibition of breathing associated with gallbladder stimulation in dogs

The effect of mechanical stimulation of the gallbladder on breathing was studied in anesthetized spontaneously breathing dogs. Measurements of tidal volume, breathing frequency, rib cage and abdominal diameter, transdiaphragmatic pressure, and electrical activity of the diaphragm were made while traction or compression was applied to the gallbladder for periods of 30 s. Both forms of mechanical stimulation produced similar changes, including large decreases in tidal volume, respiratory rate, electrical activity of the diaphragm, and transdiaphragmatic pressure swings. Inspiratory rib cage expansion was little affected, but abdominal expansion was greatly reduced, and swings in gastric pressure were reduced more than swings in pleural pressure, indicating a selective decrease in diaphragmatic activity. Recovery of all measured parameters returned toward control values, despite continued traction or compression. Some inhibition persisted after the stimulus was withdrawn. The very brief interval between stimulus and response suggested that the mechanism was a neural reflex. The afferents involved are unknown but are not purely vagal in nature, since qualitatively similar results were seen in animals after vagotomy. The alteration in breathing frequency indicates that at least part of the reflex is supraspinally mediated. The change in pattern of breathing closely resembles that seen in subjects after abdominal surgery and supports the theory that reflex inhibition of breathing contributes to postoperative pulmonary complications seen in those subjects.     

Labetalol: potent antihypertensive agent that blocks both alpha- and beta-adrenergic receptors.

Labetalol was administered as the sole antihypertensive agent to 20 ambulatory patients with mild to moderate hypertension. The mean systolic and diastolic blood pressures (+/- standard error of the mean) with the patients sitting fell significantly (P < 0.001), from 145.5 +/- 3.2 and 103.7 +/- 1.6 mm Hg respectively at the start of labetalol therapy (after a period free of antihypertensive medication) to 125.7 +/- 2.0 and 87.2 +/- 1.1 mm Hg by the end of the trial. The diastolic blood pressure was well controlled (90 mm Hg or less) with labetalol therapy in 90% of the patients. The medication was well tolerated, and no orthostatic fall in the diastolic blood pressure was observed. Pharmacologically labetalol most closely resembles a combination of a nonselective beta-adrenergic blocker like propranolol and a postsynaptic alpha-adrenergic blocker like prazosin.     

The characteristics of the alpha-adrenergic regulation of the cardiovascular system in middle-aged and elderly subjects]

97 practically healthy young adult, elderly and old people were examined to study the age-associated changes in alpha-adrenergic regulation of the cardiovascular system. The values of central and renal hemodynamics, systolic and diastolic cardiac functions, skin and bulbar microcirculation and arterial blood pressure were determined in dynamics after injection of the alpha-stimulator phenylephrine (0.15 mg/kg of body mass intramuscularly) or alpha-blocker prazosin (0.015 mg/kg of body mass orally). In old age alpha-adrenergic effects on the heart were found to decrease. In elderly and old people the changes of peripheric blood circulation prevail in the structure of hemodynamic shifts arising in stimulation and alpha-adrenergic receptors blockage.