VASOPRESSIN RELEASE DURING VENTRICULO-CISTERNAL PERFUSION WITH PROSTAGLANDIN E2 IN THE DOG

1976 ◽  
Vol 71 (3) ◽  
pp. 325-331 ◽  
Author(s):  
MANABU YAMAMOTO ◽  
L. SHARE ◽  
R. E. SHADE
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Plasma Concentrations ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
Prostaglandin E ◽  
Temperature Plasma ◽  
Vasopressin Release ◽  
Control Value ◽  
Arterial Blood

SUMMARY In an attempt to determine whether prostaglandin E2 (PGE2) can act centrally to affect the release of vasopressin (ADH), the ventriculo-cisternal system of anaesthetized dogs was perfused with PGE2. When PGE2 was perfused at a rate of 76·4 ng/min (0·19 ml/min), the plasma ADH concentration was unchanged. However, perfusion of PGE2 at a rate of 152·8 ng/min (0·19 ml/min) resulted in a significant increase in the plasma ADH concentration from the control value of 9·0 ± 2·2 (s.e.m.) to 18·8 ± 3·9 μu./ml at 10 min and to 41·0 ± 16·7 μu./ml at 30 min after the start of the perfusion. There were no changes in arterial blood pressure, rectal temperature, plasma osmolality, and the plasma concentrations of sodium and potassium. In additional experiments, i.v. injection of indomethacin (2 or 20 mg/kg) decreased the plasma ADH concentration by approximately 50%. Although this finding is consistent with a role of PGE2 in the control of ADH release, it could also have been due to the observed increases in arterial blood pressure and effective left atrial pressure. Plasma renin activity was unchanged in the indomethacin experiments. It is concluded that PGE2 can act in the central nervous system to stimulate ADH release.

Inhibition of cGMP-specific phosphodiesterase type 5 reduces sodium excretion and arterial blood pressure in patients with NaCl retention and ascites

2005 ◽  
Vol 288 (5) ◽  
pp. F1044-F1052 ◽  
Author(s):  
Helle C. Thiesson ◽  
Boye L. Jensen ◽  
Bente Jespersen ◽  
Ove B. Schaffalitzky de Muckadell ◽  
Claus Bistrup ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Sodium Excretion ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Sodium Balance ◽  
Ang Ii ◽  
Double Blind ◽  
Arterial Blood ◽  
Phosphodiesterase Type

In the present study, we tested the hypothesis that inhibition of renal phosphodiesterase type 5 (PDE5) in patients with liver cirrhosis and ascites increases sodium excretion. The effect of sildenafil citrate was studied in a randomized double-blind. placebo-controlled crossover study. Diuretics were withdrawn, and a fixed sodium diet (100 mmol/day) was given to the patients for 5 days before both study days. After a 60-min basal period, eight patients received either oral sildenafil (50 mg) or placebo. Glomerular filtration rate (GFR) and renal blood flow (RBF) were determined by 99mTc-diethylenetriamine-pentaacetate and 131I-hippuran clearances. In human nephrectomy specimens, PDE5 mRNA was expressed at similar levels in the cortex ( n = 6) and inner medulla ( n = 4). Histochemical staining showed PDE5 immunoreactivity in collecting ducts and vascular smooth muscle. At baseline, cirrhotic patients exhibited elevated plasma concentrations of ANP, renin, ANG II, and aldosterone that did not differ on the 2 study days. Basal sodium excretion was similar at the 2 study days (median 17 and 18 mmol, respectively), and patients were in positive sodium balance. Sildenafil increased heart rate, plasma renin activity, plasma ANG II, and aldosterone concentrations significantly after 60 min. Plasma cGMP concentration was increased after 120 and 180 min, and urinary sodium excretion and mean arterial blood pressure were decreased significantly at 120 and 180 min. Plasma ANP concentration, GFR, and RBF did not change after sildenafil. In patients with ascites and cirrhosis, inhibition of PDE5 did not promote natriuresis but led to increased plasma levels of the renin-angiotensin-aldosterone system.

Enhancement of the Antihypertensive Effect of Hydrochlorothiazide in Dogs after Suppression of Renin Release by Beta-Adrenergic Blockade

1975 ◽  
Vol 48 (2) ◽  
pp. 147-151
Author(s):  
C. S. Sweet ◽  
M. Mandradjieff
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Arterial Blood Pressure ◽  
Antihypertensive Effect ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Antihypertensive Activity ◽  
Adrenergic Blockade ◽  
Arterial Blood

1. Renal hypertensive dogs were treated with hydrochlorothiazide (8−2 μmol/kg or 33 μmol/kg daily for 7 days), or timolol (4.6 μmol/kg daily for 4 days), a potent β-adrenergic blocking agent, or combinations of these drugs). Changes in mean arterial blood pressure and plasma renin activity were measured over the treatment period. 2. Neither drug significantly lowered arterial blood pressure when administered alone. Plasma renin activity, which did not change during treatment with timolol, was substantially elevated during treatment with hydrochlorothiazide. 3. When timolol was administered concomitantly with hydrochlorothiazide, plasma renin activity was suppressed and blood pressure was significantly lowered. 4. These observations suggest that compensatory activation of the renin-angiotensin system limits the antihypertensive activity of hydrochlorothiazide in renal hypertensive dogs and suppression of diuretic-induced renin release by timolol unmasks the antihypertensive effect of the diuretic.

Factors associated with vasopressin release in exercising swine

1994 ◽  
Vol 266 (1) ◽  
pp. R118-R124 ◽  
Author(s):  
C. L. Stebbins ◽  
J. D. Symons ◽  
M. D. McKirnan ◽  
F. F. Hwang
Keyword(s):  
Plasma Volume ◽  
Plasma Concentrations ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
Treadmill Running ◽  
Maximal Heart Rate ◽  
Ang Ii ◽  
Strong Correlations ◽  
Vasopressin Release ◽  
Lysine Vasopressin

This study examined the effect of dynamic exercise on vasopressin release in the miniswine and factors that may elicit this response (n = 15). Thus lysine vasopressin (LVP), the catecholamines epinephrine and norepinephrine (EPI and NE), plasma renin activity (PRA), and plasma volume, Na+, and osmolality were measured before and during treadmill running at work intensities of 60, 80, and 100% of each swine's maximal heart rate reserve (HRR). LVP increased in a progressive manner similar to that of humans, ranging from 5.9 +/- 0.4 pg/ml before exercise to 30.1 +/- 4.5 pg/ml during maximal exercise. EPI, NE, and PRA [an index of angiotensin II (ANG II) activity] demonstrated a pattern of response comparable to LVP. Although these hormones can influence the release of LVP, only PRA displayed a strong correlation with LVP (r = 0.84). When ANG II synthesis was blocked (captopril, 1-3 mg/kg, intra-atrial injection) during exercise (80% HRR), plasma LVP was reduced from 9.9 +/- 0.6 to 7.5 +/- 0.6 pg/ml (P < 0.05). In addition, moderate-to-strong correlations were found between plasma concentrations of LVP and plasma osmolality (r = 0.79) and body temperature (r = 0.78). Plasma LVP also correlated with decreases in plasma volume (r = 0.84). These data suggest that the miniswine model is a good one for studying vasopressin effects during exercise and that ANG II appears to be a particularly strong stimulus for the release of this hormone.

Interactions between brain acetylcholine and prostaglandins in control of vasopressin release

1991 ◽  
Vol 261 (2) ◽  
pp. R420-R426
Author(s):  
M. Inoue ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion ◽  
Stimulation Of

We have examined in conscious rats the interaction between centrally acting prostanoids and acetylcholine in the stimulation of vasopressin secretion. The intracerebroventricular (icv) administration of carbachol (25 ng) resulted in marked transient increases in the plasma vasopressin concentration and mean arterial blood pressure and a transient reduction in heart rate. Central cyclooxygenase blockade by pretreatment icv with either meclofenamate (100 micrograms) or indomethacin (100 micrograms) virtually completely blocked these responses. Prostaglandin (PG) D2 (20 micrograms icv) caused transient increases in the plasma vasopressin concentration (much smaller than after carbachol) and heart rate, whereas mean arterial blood pressure rose gradually during the 15-min course of the experiment. Pretreatment with the muscarinic antagonist atropine (10 micrograms icv) decreased the peak vasopressin response to icv PGD2 by approximately one-third but had no effect on the cardiovascular responses. We conclude that the stimulation of vasopressin release by centrally acting acetylcholine is dependent on increased prostanoid biosynthesis. On the other hand, stimulation of vasopressin release by icv PGD2 is partially dependent on activation of a cholinergic pathway.

Hormonal responses to synthetic atrial natriuretic peptide in patients on regular hemodialysis

1988 ◽  
Vol 119 (2) ◽  
pp. 257-262 ◽  
Author(s):  
Sadao Nakajima ◽  
Hiromichi Suzuki ◽  
Yo Kageyama ◽  
Takashi Takita ◽  
Takao Saruta
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Arterial Blood ◽  
Sympathetic Nervous ◽  
Regular Hemodialysis

Abstract. The effects of atrial natriuretic peptide (ANP) on mean arterial blood pressure, heart rate, plasma renin activity, aldosterone, cortisol, norepinephrine, epinephrine and arginine vasopressin were studied in 6 anuric subjects receiving regular hemodialysis. An iv bolus injection of 8 nmol of ANP followed by infusion at 32 pmol·kg−1·min−1 for 1 h in the pre- and posthemodialysis period was performed. Basal plasma ANP was higher before than after hemodialysis. ANP administration produced a reduction in mean arterial blood pressure accompanied by an elevation of norepinephrine and of plasma renin activity (from 2.49 ± 0.52 to 3.39 ± 0.85 nmol·l−1·h−1 predialysis and from 2.78 ± 0.71 to 3.15 ± 0.86 nmol·l−1·h−1 postdialysis, respectively, mean ± sem; P < 0.05). Plasma aldosterone and cortisol were significantly decreased. Plasma epinephrine and AVP remained unchanged. These hemodynamic and hormonal changes were similar in the pre- and the postdialysis period. These results suggest that 1) ANP causes a fall in mean arterial blood pressure, which in turn induces reflex tachycardia and activation of the sympathetic nervous system without diuresis; 2) the activated sympathetic nervous system as reflected in elevation of plasma norepinephrine may increase plasma renin activity; 3) reduced plasma aldosterone is not influenced by enhancement of the reninangiotensin system; therefore, 4) reduction of plasma aldosterone as well as cortisol is probably due to direct action of ANP, and finally 5) AVP had no direct relation with ANP administration.

Rapid effects of parathyroid hormone(1–34) and prostaglandin E2 on bone blood flow and strontium clearance in the rat in vivo

1991 ◽  
Vol 131 (3) ◽  
pp. 359-365 ◽  
Author(s):  
E. Cochrane ◽  
I. D. McCarthy
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Parathyroid Hormone ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Prostaglandin E ◽  
Bone Blood Flow ◽  
Vascular Effects ◽  
Arterial Blood ◽  
Mineral Ions

ABSTRACT The vascular effects of noradrenaline, ATP, parathyroid hormone (PTH) and prostaglandin E2 (PGE2) were investigated in the rat. Additionally, the exchange of mineral ions between bone and blood was assessed by measuring strontium clearance, with the aim of investigating whether the vascular effects of these agents altered uptake of mineral ions or if this exchange could be changed independently of blood flow. Radioactive microspheres and 85Sr were used to establish bone blood flow and mineral clearance. Measurements of bone blood flow and arterial pressure were made in each animal and used to calculate vascular resistance. A measurement of 85Sr clearance was also obtained. Arterial blood pressure was significantly affected by noradrenaline (P ≤ 0·003) and ATP (P ≤ 0·015). Additionally, noradrenaline significantly (P ≤ 0·03) reduced bone blood flow. This decrease was related to a significant increase in vascular resistance. Arterial blood pressure and bone blood flow were significantly reduced by both bovine PTH(1–34) (P ≤ 0·001, P ≤ 0·02) and PGE2 (P ≤ 0·005, P ≤ 0·001). Vascular resistance to bone was increased by both agents but this was only statistically significant in the case of PGE2 (P ≤ 0·01). A significant (P ≤ 0·001) reduction in strontium was also produced by PGE2. In each group the relationship between bone blood flow and strontium clearance was then analysed. Only the PGE2-treated group had a slope of the regression which was statistically different from both the control animals and the other drug-treated groups. Treatment with PGE2 therefore resulted in a dose-related decrease in 85Sr clearance which was not related to the reduction in bone blood flow. Journal of Endocrinology (1991) 131, 359–365

Arterial baroreceptors mediate the inhibitory effect of acute increases in arterial blood pressure on thirst

2002 ◽  
Vol 282 (6) ◽  
pp. R1718-R1729 ◽  
Author(s):  
Sean D. Stocker ◽  
Edward M. Stricker ◽  
Alan F. Sved
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Drinking Behavior ◽  
Plasma Osmolality ◽  
Inhibitory Effect ◽  
Ang Ii ◽  
Arterial Blood ◽  
Acute Increase ◽  
Behavior Of Rats ◽  
Arterial Baroreceptor

The present study sought to determine whether arterial baroreceptor afferents mediate the inhibitory effect of an acute increase in arterial blood pressure (AP) on thirst stimulated by systemically administered ANG II or by hyperosmolality. Approximately 2 wk after sinoaortic denervation, one of four doses of ANG II (10, 40, 100, or 250 ng · kg−1 · min−1) was infused intravenously in control and complete sinoaortic-denervated (SAD) rats. Complete SAD rats ingested more water than control rats when infused with 40, 100, or 250 ng · kg−1 · min−1 ANG II. Furthermore, complete SAD rats displayed significantly shorter latencies to drink compared with control rats. In a separate group of rats, drinking behavior was stimulated by increases in plasma osmolality, and mean AP was raised by an infusion of phenylephrine (PE). The infusion of PE significantly reduced water intake and lengthened the latencies to drink in control rats but not in complete SAD rats. In all experiments, drinking behavior of rats that were subjected to sinoaortic denervation surgery but had residual baroreceptor reflex function (partial SAD rats) was similar to that of control rats. Thus it appears that arterial baroreceptor afferents mediate the inhibitory effect of an acute increase in AP on thirst stimulated by ANG II or hyperosmolality.

Regulation of fetal placental blood flow in the lamb

1984 ◽  
Vol 247 (3) ◽  
pp. R567-R574 ◽  
Author(s):  
D. F. Anderson ◽  
J. J. Faber
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Fetal Growth ◽  
Control Value ◽  
Flow Restriction ◽  
Arterial Blood ◽  
Placental Blood ◽  
Carotid Arterial ◽  
Placental Blood Flow

Inflatable occluders were placed on the distal aorta of 11 fetal lambs. After 1 wk of control measurements, fetal placental blood flow was reduced to about two-thirds of its control value for an average period of 2 wk. No allowance was made for fetal growth. During the period of flow restriction, fetal growth was 2%/day. Femoral arterial blood pressure was reduced from a control value of 41 to 27 mmHg (P less than 0.001). There was an insignificant increase in carotid arterial blood pressure from 48 to 50 mmHg. Placental resistance to flow did not decrease more than could be accounted for by the increase in gestational age in the course of the experiment. It is concluded that fetal placental blood flow is not under feedback control, since neither of the determinants of flow (i.e., driving pressure and resistance) responded to its chronic reduction.

Sign in / Sign up

Export Citation Format

Share Document