Evidence from a dual action of converting enzyme inhibitor on blood pressure in normal man

We studied the effect of a converting enzyme inhibitor (CEI), Captopril SQ 14,225 50 mg p.o. in eight supine normal subjects under a high sodium (150 meq/d) and low sodium (25 mEq/d) diet. On high sodium, plasma renin (PRA) and aldosterone were basal and Saralasin did not lower mean blood pressure. However, CEI induced an 11.4±3.2 mm fall in blood pressure (p<0.02) and either indomethacin 50 mg or ibuprofen 800 mg (PI), when given simultaneously on another day, abolished the blood pressure response (2.5±0.9 mm Hg, p>0.5). In contrast, on a low salt diet where renin was increased, CEI induced a drop in blood pressure which was not significantly altered by PI (12.8±1.1 vs. 10.0±3.1 mm Hg, p>0.5). CEI increased plasma renin on both diets (1.7±0.5 to 3.5±0.8 and 2.8±0.6 to 12.5±3.1 ng/ml/hr respectively both p<0.05). Aldosterone did not change (high Na⁺) or fell (low Na⁺). Inhibition of prostaglandin synthesis did not significantly block the renin rise from CEI suggesting that the direct angiotensin II negative feedback is relatively independent of acute prostaglandin release. Our studies suggest that CEI has a dual hypotensive action. In a low renin state, the hypotensive action appears to be mediated through vascular prostaglandins.     

Influence of adrenergic nervous and prostaglandin systems on hydralazine-induced renin release

The role of the beta-adrenergic nervous and prostaglandin systems in vasodilator-induced activation of the renin-angiotensin system was studied in conscious rats. The plasma renin activity (PRA) response to intravenous hydralazine (0.25, 0.5 and 1 mg/kg body wt.) was compared to the PRA response following administration of similar doses of hydralazine to rats pretreated with either indomethacin (3 mg/kg body wt. i.v.) or indomethacin and propranolol (1 mg/kg body wt. i.v.). PRA increased significantly above control levels after each of the hydralazine doses. In rats pretreated with indomethacin, PRA did not increase with the 0.25 mg/kg dose of hydralazine; increased significantly with the 0.5 mg/kg dose but remained significantly lower than the PRA response in the absence of indomethacin; and increased with the 1 mg/kg dose to a level not significantly different from PRA in rats receiving only hydralazine. When rats were pretreated with indomethacin and propranolol, PRA did not increase significantly in response to either the 0.25 or 0.5 mg/kg doses of hydralazine. Although a statistically significant increase in PRA was noted with the 1 mg/kg dose of hydralazine, the level of PRA achieved was very low and only 15% of that observed with the other two treatment regimens (i.e., hydralazine alone or indomethacin and hydralazine). These results demonstrate that vasodilator-induced renin release is only partially mediated via the prostaglandin system, that the degree of this control is related to the intensity of vasodilator stimulus and that renin release following administration of hydralazine can be attributed almost entirely to activation of the beta-adrenergic nervous and prostaglandin systems.     

Effects of moderate short-term potassium depletion in normal humans the role of prostaglandins

The role of prostaglandins (PG) in the effects of potassium (K⁺)depletion was studied in six normal women. A mean K⁺-deficit of 220 mEq was induced with and without concomitant treatment with indomethacin (150 mg/day). Mean serum K⁺ concentration decreased from 4.2 ± (S.E.) 0.1 to 3.2 ± 0.1 mEq/L without indomethacin and from 4.1 ± 0.1 to 3.2 ± 0.1 mEq/L with indomethacin. “Supine” and “upright” plasma renin activity (PRA) and plasma norepinephrine concentration (NE) were unaltered by K⁺ -depletion alone but decreased with indomethacin. Plasma aldosterone (PA) was suppressed during K⁺-depletion (control: 7.2 ± 2.6 ng/dl supine, 19.3 ± 8.1 ng/dl upright; K⁺-depletion: 2.6 ± 0.3 ng/dl supine, 5.5 ± 1.3 ng/dl upright) and was paralleled by a decrease in urinary aldosterone. K⁺-depletion decreased urinary PGE₂ from 667 ± 133 to 343 ± 60 ng/day (P < 0.025) without a change in PGF₂. The dose of exogenous angiotensin II (A II) which increased diastolic blood pressure by 20 mm Hg (pressor dose) was 7.1 ± 1.4 ng/kg/min during control and increased to 11.0 ± 0.7 ng/kg/min during K⁺-depletion (P < 0.05). Indomethacin increased the sensitivity to A II both during control (pressor dose: 4.9 ± 0.6 ng/kg/min) and K⁺- depletion (pressor dose: 6.0 ± 1.0 ng/kg/min). These results indicate that in healthy subjects, moderate short-term K⁺-depletion does not affect PRA or NE but decreases production of aldosterone and PGE₂ by the kidney. The changes in vascular sensitivity to exogenous A II during K⁺-depletion and indomethacin and the decreases in plasma NE and PRA during indomethacin may be explained by changes in vascular vasodilator PG.     

Role of antidiuretic activity in the inhibition of renin secretion by vasopressin in anesthetized dogs

The nature of the activity of vasopressin which is responsible for the inhibition of renin secretion was studied by comparing the effects of vasopressin (AVP) and analogs of AVP in anesthetized water-loaded dogs. Infusion of AVP (1.0 ng/kg/min) increased mean arterial pressure (MAP) and decreased heart rate (HR) and free water clearance (CH2O). Plasma renin activity (PRA) decreased from 11.9 +/- 4.7 to 3.8 +/- 1.7 ng/ml/3 hr (p less than 0.05). A selective antidiuretic agonist, 1-deamino-8-D-arginine vasopressin (1.0 ng/kg/min), which had no effect on MAP or HR but was effective as AVP in decreasing CH2O, decreased PRA from 13.5 +/- 4.6 to 7.0 +/- 2.9 ng/ml/3 hr (p less than 0.05). Infusion of a selective vasoconstrictor agonist, 2-phenylalanine-8-ornithine oxytocin (1.0 ng/kg/min), increased MAP and decreased HR but did not decrease CH2O or PRA. A vasoconstrictor antagonist, d(CH2)5Tyr(Me)AVP (10 micrograms/kg), completely blocked the MAP and HR responses to AVP but did not block the decrease in CH2O or PRA (5.9 +/- 1.8 to 2.9 +/- 1.6 ng/ml/3 hr) (p less than 0.001). Infusion of the 0.45% saline vehicle had no significant effect on MAP, HR, CH2O or PRA. These results indicate that the inhibition of renin secretion by vasopressin in anesthetized water-loaded dogs is due to its antidiuretic activity.     

Effect of storage time and temperature on steroid and protein hormone concentrations in porcine plasma and serum

The effect of storage time and temperature of porcine blood prior to quantitation of hormone concentrations by radioimmunoassay (RIA) was evaluated. Blood from each of four luteal phase gilts was used to determine cortisol (CS) and progesterone (P) concentrations, while blood from each of four ovariectomized gilts and each of four lactating sows was used to determine luteinizing hormore (LH) and prolactin (PRL) concentrations, respectively. Blood was collected via jugular puncture from each animal within a 30-sec time period and placed into 18 heparinized and 18 nonheparinized tubes. One sample with and without heparin was stored in ice water (4°C) or at 28°C for 0.25, 2, 4, 6, 8, 12, 24, 36 or 48 hours. After storage, blood was centrifuged at 4°C and plasma or serum was collected and stored at ?20°C until quantitated by RIA. There were no differences (P>0.05) between plasma and serum concentrations (X ± SE, ng/ml) of CS (26.9 ± 0.8 vs 28.5 ± 0.8), P (24.7 ± 0.7 vs 24.8 ± 0.8), LH (2.1 ± 0.1 vs 2.2 ± 0.1) or PRL (53.2 ± 2.3 vs 52.6 ± 2.1). Similarly, storage temperature (4 vs 28°C) did not affect the concentrations of P (25.7 ± 0.8 vs 23.9 ± 0.7), LH (2.2 ± 0.1 vs 2.2 ± 0.1) or PRL (53.7 ± 2.1 vs 53.2 ± 2.3). Howver, CS concentrations decreased (P<0.05) from 28.5 ± 0.5 (4°C) to 26.9 ± 0.8 ng/ml (28°C). There was an animla x time interaction for CS concentration when plasma and serum were stored at both 4°C (P<0.001) and 28°C (P<0.003). There was also and animal x time interaction (P<0.03) for LH concentrations. The P and PRL concentrations decreased linearly by 0.0615 ng/hr (P<0.001) and 0.0625 ng/hr (P<0.004), respectively, with increased storage time.     

Suppression of renin secretion by propranolol in salt-depleted dogs

d, 1-propranolol was infused into salt-depleted, conscious dogs at two dosages: 1 mg/kg followed by 0.60 ? 0.67 mg/kg/hr, and 5 mg/kg followed by 1.57 ? 1.76 mg/kg/hr. At both dosages, propranolol decreased plasma renin activity (PRA), plasma aldosterone concentration, and heart rate significantly. Renin substrate concentration remained unchanged. PRA was suppressed with the higher dosage but not with the lower dosage, to values found with dietary salt loading. Mean arterial blood pressure (MABP) remained unchanged with the low-dose infusions, but decreased significantly with the high-dose infusions. The data suggest that the mechanism(s) for the increase in PRA with low-salt diets is sensitive to propranolol and that the effect of propranolol on MABP is dependent on the salt intake and on the dose administered.     

Antitesticular activity of DL-6-(N-2-Pipecolinomethyl)-5-Hydroxy-Indane maleate (PMHI) in coyotes (canis latrans)

The ban on toxicants for coyote control has created a need for alternative control methods. Reproductive inhibitors may provide a means of maintaining coyote populations at levels where impact on live-stock is acceptable. Therefore, the effects of PMHI on testicular activity of coyotes were evaluated. Twelve mature, male coyotes were weighed and allotted randomly to 1 of 4 treatment groups: (1) controls, (2) 5, (3) 10, and (4) 20 mg PMHI/kg body weight (BW). PMHI was dissolved in 2 ml distilled water and ethanol (1:1) and administered as a single sc injection. All coyotes were observed for 1 hr after treatment and any adverse effects recorded. Fifteen days after treatment, a testicle and epididymis from each coyote was selected at random, ablated, weighed, fixed in formalin, and prepared for histologic examination. The remaining testicle was prepared similarly 30 days post-treatment. Data were analyzed by a balanced factorial in a split-plot arrangement. Unlike controls, coyotes given PMHI exhibited signs of nausea and diarrhea within 15 to 30 min, which subsided after 45 to 60 min. PMHI temporarily increased (P<.01) serum glutamic-pyruvate transaminase (SGPT) but did not alter other blood chemistry or hematologic values. PMHI reduced (P<.01) testicular weights (wet weights) from 10±1.0 g (controls) to 6.3±0.2 g after 5 mg, 4.4±0.2 g after 10 mg, and 6.0±0.5 g after 20 mg/kg BW. Testicular weights were not different among the 3 treatments of PMHI. Histological changes in seminiferous tubules were consistent with absence of spermatogenesis at 15 and 30 days after all treatment levels of PMHI. Only occasional intact spermatozoa were present in sections of epididymis at 15 and 30 days after PMHI treatment. We conclude that PMHI may cause infertility in the male coyote from 15 to at least 82 days after treatment without apparent chronic damage to vital organs.     

Effects of a nonperssor analogue of vasopressin on plasma renin activity and salt and water excretion in water-loaded,anesthetized dogs

The object of this study was to determine the importance of vasoconstrictor activity in the suppression of renin secretion by vasopressin. Arginine vasopressin (AVP) (0.05 and 0.1 ng/kg/min) and a nonpressor analogue of vasopressin, 1-deamino-[4-threonine, 8-D-arginine]-vasopressin (dTDAVP) (0.01 and 0.05 ng/kg/min), were infused intravenously in anesthetized hypophysectomized dogs. Neither dTDAVP nor AVP influenced arterial pressure or heart rate but both suppressed plasma renin activity. Infusion of dTDAVP at 0.01 and 0.05 ng/kg/min suppressed plasma renin activity to 86±4% (p<0.05) and 63±6% (p<0.01) of the control values respectively. Infusion of AVP at 0.05 and 0.1 ng/kg/min suppressed plasma renin activity to 60±8% (p<0.01) and 59±12% (p<0.05) of the central values respectively. dTDAVP and AVP both produced significant increases in sodium excretion. These data demonstrate that vasoconstrictor activity is not required for the effects of vasopressin on renin secretion and sodium excretion.     

Preparturient changes in plasma concentrations of estrone,estradiol-17β and estradiol-17α in the fetal calf: Effects of dexamethasone infusion

The concentrations of total estrogens in fetal calf plasma were determined during a 6–10 day period immediately before delivery. Comparison was made between levels found in untreated calves and calves infused with dexamethasone at the rate of 0.1, 1.0 and 10 mg/24 hours. In untreated calves the plasma estrone, estradiol-17β and estradiol-17α levels remained relatively constant at 38 ± 7 ng ml^?1 (mean ± SEM n = 3), 46 ± 6 ng ml^?1 and 29 ± 5 ng ml^?1 respectively. Infusion with dexamethasone at 0.1 mg/24 hr (3 calves) and 1.0 mg/24 hr (3 calves) was without dramatic effect on plasma estrogen levels. However, in one fetus infused with 10.0 mg/24 hr the dexamethasone treatment may have caused a transitory rise in the levels of all estrogens examined.     

Effect of prostaglandin E1 on renin and aldosterone in hypertensive patients.

The effect of prostaglandin E1 (PGE1) on plasma renin activity (PRA) and plasma aldosterone concentration (PAC) was studied in the hypertensive subjects treated with or without 75 mg indomethacin or 60 mg propranolol for a week. Subsequent to the treatment with indomethacin for a week, PRA and PAC levels were decreased as compared to the control, without changes in the blood pressure and heart rate. During the infusion of PGE1, the blood pressure was decreased and the pulse rate was increased. PRA and PAC levels were also elevated. These changes of parameters were not different between the control and the indomethacin-treated subjects. PRA and PAC were suppressed after the treatment with propranolol. With the infusion of PGE1, the level of PRA was not significantly elevated, while, PAC was significantly increased by the infusion of 100 ng/Kg/min of PGE1. During the infusion of PGE1, the blood pressure was decreased while the pulse rate was increased in the subjects treated with propranolol. However, the elevation of the pulse rate was less remarkable than the control. These data indicate that PGE1 have important roles in the regulation of the release of renin and aldosterone. These findings also suggest that PGE1 may act to stimulate the secretion of aldosterone in man.     

The study of renin–angiotensin–aldosterone in experimental diabetes mellitus

It is generally accepted that hypertension and other vascular pathologies increase in diabetes mellitus (DM) patients as a result of the renin–angiotensin–aldosterone (RAA) system. In this study, changes in the renin‐angiotensin‐aldosterone (RAA) system level was determined in Streptozotocin (STZ)‐injected rats. A total of 46 female Wistar albino rats (180–220 g body weight) was utilized in these experiments. STZ was given intraperitoneally to induce diabetes in rats. Streptozotocin (60 mg kg⁻¹ body weight) was dissolved in 0·1 m citrate–‐phosphate buffer (pH 4–5). The non‐diabetic rats were injected with sterilized buffer alone to act as a control group. Blood glucose levels were 398±8·2 mg dl⁻¹, 488±11·75 mg dl⁻¹ and 658±29·6 mg dl⁻¹ at days 3, 12 and 30 respectively. The level of plasma renin activity (PRA) was measured as 7·69±1·07 ng ml⁻¹ h⁻¹; 1·82±0·22 ng ml⁻¹ h⁻¹ and 0·67±0·12 ng ml⁻¹ h⁻¹ at days 3, 12 and 30, respectively. These values showed that the PRA levels are decreased with increased time period. Serum angiotensin converting enzyme (ACE, E.C. 3.4.15.1) levels were increased at days 12 and 30 (p<0·05 and p<0·005), whereas serum aldosterone levels were increased at days 3 and 12 (p<0·05). The level of urea and creatinine increased at days 12 and 30 (p<0·05 and p<0·005, respectively) when compared to the control group. The data from these experiments indicate that the PRA level decreased whereas ACE activity level increased in diabetic rats compared with the control. Aldosterone levels increased at the first stage of the experiment, but then decreased by the end of the experiment as a result of changes in renin and ACE levels. Copyright © 1999 John Wiley & Sons, Ltd.     

Effect of monensin and suckling on the GnRH induced luteinizing hormone surge and the effect of monensin on the postpartum interval in Brangus cows

Twenty-seven fall calving Brangus cows were randomly allotted to one of four treatment groups: nonsuckled monensin (NSM), suckled monensin (SM), nonsuckled control (NSC), and suckled control (SC). Cows were group fed 1.82 kg/hd/day concentrate and Coastal bermuda grass hay $\text{ad}$$\text{libitum}$. Monensin cows received 200 mg monensin/hd/day in the concentrate. At 0800 hr on day 21 postcalving, the calves were separated from the cows. Suckled monensin and SC cows were allowed to suckle their calves for 30 min at 6-hr intervals. Nonsuckled monensin and NSC cows were not suckled. Calves were given free access to the cows after 1400 hr on day 22 postpartum. At 0800 hr on day 22 postpartum, a blood sample was collected. A 100 μg GnRH challenge was administered IM at 0801 hr. Blood samples were collected at 15-min intervals for 6 hr postinjection. Changes in body weight and body condition from day 21 postpartum to the day of first estrus were not different (P>0.10) by dietary treatment. Monensin cows consumed 10.7% less hay than did the control cows. Serum luteinizing hormone (LH) following GnRH was greater (P<0.005) in suckled than nonsuckled cows. Control cows released more (P<0.005) LH in response to GnRH than did the monensin cows. The postpartum interval (to first estrus) for the monensin cows (92.4±14.7 days) was shorter (P<0.025) than the controls (138.5±9.5 days). A greater proportion (P<0.005) of the monensin cows (8 of 14) exhibited estrus by 90 days postpartum compared to the control cows (0 of 13). Monensin and suckling appear to exert independent and agonistic influences on pituitary function in the postpartum beef cow.     

Luteinizing hormone,total estrogens and progesterone secretion during lactation and after weaning in sows

Two experiments were conducted to determine changes in serum concentrations of LH, total free estrogens and progesterone before and after weaning in sows. Blood was collected either via indwelling anterior vena cava cannula or by venipuncture and serum hormones were measured by radioimmunoassay. In Exp. I, blood was collected at 15-min intervals for 4 hr on day 7 and day 21 postpartum from three sows on each day. In addition, individual samples were collected from 10 sows on days 4 and 14 postpartum and from 11 sows on days 1, 3 and 5 after weaning (day 23 postpartum). Serum LH ranged from .2 to .8 ng/ml during lactation and averaged 1.1 ± .7, 1.1 ± .7 and 2.7 ± .7 on days 1, 3 and 5 after weaning, respectively. Progesterone was low (< 1 ng/ml) during lactation and averaged 1.9 ± .3, .6 ± .3 and 1.2 ± .3 on days 1, 3 and 5 after weaning. Estrogens were variable during lactation, averaged 121 ± 36 pg/ml on day 1 after weaning and decreased thereafter. Estrus began on day 3 after weaning in 1 sow and on day 5 in the remaining 10 sows.In Exp. II, blood was collected from seven sows at 12 to 24 hr intervals from 2 days before until 5 days after weaning (day 26 postpartum). Mean serum LH was .7 ± .1 ng/ml during 48 hr before weaning and remained unchanged after weaning until day 3 when LH increased to 6.1 ± .8 ng/ml. Serum LH concentrations then declined to 1.3 ± .8 and .9 ± .8 ng/ml on days 4 and 5 after weaning. Total estrogens averaged 31 ± 4 pg/ml during 48 hr prior to weaning and 32 ± 4, 43 ± 17, 28 ± 1, 30 ± 2, 16 ± 2 and 18 ± 2 on days 0 to 5 after weaning. Progesterone increased from 1.0 ± .3 ng/ml 24 hr before weaning to 3.0 ± .3 at weaning and then remained low (< 1 ng/ml) until after ovulation when progesterone increased. Estrus began on day 4 after weaning in all seven sows.Results from these two experiments indicate that in sows: (1) LH is suppressed during early lactation (day 7), gradually increases during late lactation (day 21) and then reaches peak concentrations after weaning near the onset of estrus, (2) estrogens increase between weaning and estrus and decline thereafter, and (3) progesterone rises transiently at weaning and then increases after estrus and ovulation.     

Alpha melanocyte stimulating hormone inhibits prolactin secretion in fetal and infant lambs

The intravenous administration of αMSH (25 μg/kg) to 11 lambs (3 to 29 days of age) suppressed plasma PRL by 15 minutes. The mean basal concentration was 15.3 ± 2.9 ng/ml and the mean nadir was 4.9 ± 0.8 ng/ml (p<0.01). In chronically catheterized fetuses (128–140 days), intravenous administration of αMSH (25 μg/kg) decreased basal PRL levels (89.6 ± 12.4 ng/ml) significantly at 15–30 minutes to levels of 74.3 ± 11.4 ng/ml (p<.01). The degree of suppression of basal PRL levels was less in fetusus (76.9 ± 4.1%) than that induced in the neonates (40.5 ± 7.1%). In younger fetuses <120 days in whom basal PRL levels are low (3.0 ± 2.1 ng/ml), administration of αMSH was without effect. Plasma GH concentrations were not altered by administration of αMSH. The suppression of PRL secretion by αMSH administration could result from increased release of hypothalamic dopamine or be a direct effect on secretion of prolactin by the pituitary.     

Ephedrine accelerates psychomotor recovery from anesthesia in macaque monkeys

Background Ephedrine is used in treatment of hypotension during anesthesia. We investigated its effects on the psychomotor recovery and its potential adverse reactions on cardiorespiratory functions in rhesus monkeys. Methods The monkeys received 50 μg/kg medetomidine, 2.0 mg/kg S‐ketamine with 150 IU hyaluronidase i.m. Pulse rate, blood pressure and saturation of haemoglobin were monitored for 20 minutes. Thereafter, 1 mg/kg of ephedrine or a placebo was administered i.m. and behavioural changes, pulse rate, blood pressure and saturation of haemoglobin were monitored every 5 minutes. Results Ephedrine shortened recovery from anaesthesia from 80.4 ± 25.8 to 14.83 ± 13.70 minutes. Ephedrine also increased oxygen saturation of haemoglobin and systolic blood pressure and caused significant decrease in pulse rate 5 minutes after its administration. Conclusions Ephedrine can be successfully used to accelerate psychomotor recovery after the use of common anesthetic protocols combining dissociative anesthetic agent and alpha 2‐adrenoceptor agonist in primates.     

Prazosin unmasks a renin response to intravenous para-chloroamphetamine

When injected intraperitoneally, p-chloroamphetamine (PCA) causes the acute release of catecholamines and serotonin, increases mean arterial pressure (MAP) and increases plasma renin activity (PRA) in rats. Experiments were designed to determine the dose-response and time-course for the effect of PCA administered intravenously on PRA in conscious, unrestrained rats. It was found initially that intravenous doses of PCA ranging from 0.3 - 6.0 mg/kg caused rapid and marked hypertension, but produced variable effects on PRA for up to 30 minutes after injection. In a second study PCA (0.3 - 6.0 mg/kg) did not alter PRA at 30 or 60 minutes after intravenous injection, but did increase PRA 60 minutes after 10 mg/kg, intraperitoneally. When the hypertension elicited by intravenous PCA was abolished by pretreatment with the alpha 1-adrenoceptor antagonist prazosin (100 micrograms/kg, iv), PCA produced marked elevations in PRA from 15 - 60 minutes. Thus it appeared that the renin response to intravenous PCA was masked by an elevation in MAP; when the vascular response to PCA was blocked, a large increase in PRA was observed.     

Prostaglandin F2α (PGF2α) and prolactin secretion in rats

Plasma prolactin and F-prostaglandins (PGF) were measured in anesthetized male Sprague-Dawley rats before and at 15, 30, 45 and 60 minutes following i.v. injection of either PGF_2α (4 mg/kg), chlorpromazine, 1 mg/kg or chlorpromazine (1 mg/kg) after pretreatment with i.p. indomethacin (2 mg/kg). Following PGF_2α administration, plasma prolactin levels increased significantly only at 15 and 30 minutes in spite of extremely high PGF levels throughout 60 minutes. Besides the expected rise in plasma prolactin, chlorpromazine caused a transient but statistically significant increase in PGF. Indomethacin blocked the chlorpromazine-induced PGF rise but not prolactin increase. Animals stressed with ether anesthesia showed elevation of plasma prolactin, which was not blocked by indomethacin although PGF concentration fell. These results indicate that PGF_2α can stimulate prolactin release. This effect does not appear to be physiologic since very high PGF levels are required. Furthermore, blockade of prostaglandin synthesis by indomethacin does not prevent the release of prolactin in response to chlorpromazine or stress. Our findings do not support a possible role of PGFs as intermediaries in prolactin release. However, it is possible that PGFs may work through other mechanisms not investigated in our study.     

Effect of corticoid induced parturition on lactation and on prepartum profiles of serum progesterone and the estrogens among cows retaining and not retaining fetal membranes

Twenty-one mature F1 Brahman-Hereford cows were treated with 25 mg of dexamethasone (DEX) on day 279 or 280 of gestation to induce birth prematurely. Eigth cows were untreated (UT). Blood was sampled on day 279 or 280 of gestation just prior to treatment of cows with DEX (0 hr), at least daily thereafter to calving and within 1 hr postpartum. Concentrations of progesterone (P₄), estrone (E₁) and estradiol-17β (Eβ) and -17α (Eα) in blood serum were measured by radioimmunoassay. Among 21 cows treated with DEX, 16 (76%) calved within 78 hr (52±3 hr). Eleven of the 16 cows retained fetal membranes more than 12 hr (RFM) and five cows did not retain fetal membranes (NRFM). Five cows (24%) treated with DEX calved 266±46 hr later (NOR) on day 290±1 of gestation compared to day 286±2 for cows in group UT. No cow in groups NOR or UT had RFM. Failure of group NOR to calve prematurely appeared due to elevated serum P₄ (P<.05), low serum Eβ (P<.10) and other estrogens (P>.10) pretreatment, and to only a 32% decrease in serum P₄ within 72 hr after treatment. Serum estrogens, especially Eβ, were next lowest pretreatment in group RFM. However, in group RFM, all serum estrogens increased (P<.10 to P<.01) within 48 hr after treatment, reached higher concentrations and peaked later in relation to calving than in other groups (NRFM, NOR and UT). Synchronization of placental maturation and parturition may require a longer period of elevated serum estrogens prior to calving than was observed in group RFM. Treatment of cows prepartum with DEX had no effect on gain of calves, milk yield or yields of fat, total protein and total solids in milk during the first 12 weeks of lactation.     

Effect of L-dopa and bilateral nephrectomy on the aldosterone response to metoclopramide

The dopaminergic antagonist, metoclopramide (MCP) causes an increase in plasma aldosterone (PA) by a processnot well delineated. To investigate the mechanism of action of metoclopramide (MCP), studies were performed in rats after pre-treatment with L-dihydroxy-phenylalanine (L-dopa) and after bilateral nephrectomy. Intra-arterial MCP (200 μg/kg) resulted in a significant elevation in PA and prolactin (PRL) at 5 min and plasma renin activity (PRA) at 10 min without altering serum potassium levels. Pre-administration of L-dopa (30 mg/kg) delayed and markedly blunted PA, PRL and PRA resonses to MCP. In 7 rats, studied 30 hours after bilateral nephrectomy, the PRA was measurable (2.5 ± 0.4 ng/ml h^?1) but displayed no response to MCP. In contrast, the PA and PRL responses to MCP were not significantly affected. L-dopa induced suppression of PRA and PA was prevented by pre-administration of MCP. These results suggest that dopaminergic modulation of PA secretion occurs independently of the renin-angiotensin system.     

Effect of time and temperature on bovine serum and plasma progesterone concentration

Whole blood, with and without anticoagulant, from 5 pregnant cows was incubated at 40°C for 0 (30 minutes after collection), 6 and 24 hours (hr) before the blood was centrifuged and the plasma or serum was frozen for later progesterone assay. Mean plasma progesterone concentration decreased from 6.6 ng/ml at 0 hr to 1.7 ng/ml at 6 hr (P < 0.01) and to 2.8 ng/ml at 24 hr (P < 0.01). Mean serum progesterone concentration decreased from 6.1 ng/ml at 0 hr to 3.9 ng/ml at 6 hr (P < 0.01) and to 4.4 ng/ml at 24 hr (P < 0.01). Whole blood samples with and without EDTA were also incubated at 4°C for 24 hr. Mean plasma progesterone concentration decreased from 6.6 ng/ml at 0 hr to 4.2 ng/ml at 24 hr (P < 0.01). Mean serum progesterone concentration decreased from 6.1 ng/ml at 0 hr to 4.7 ng/ml at 24 hr (P < 0.01). The incubation time and temperature of whole blood, from collection of blood to the separation of serum or plasma, significantly affects assayable concentration of progesterone.