Hemodynamic, hormonal, and drinking responses to reduced venous return in the dog

The effect of an acute reduction in venous return, caused by reversible constriction of the thoracic vena cava, on drinking and secretion or arginine vasopressin (AVP) was examined in the dog. Plasma AVP levels rose immediately from a control level of 1.4 +/- 0.1 pg/ml (mean +/- SE) to a plateau ranging between 36 and 42 pg/ml during the first 30 min after constriction but declined to 12.6 +/- 4.2 pg/ml 2 h after constriction even though systemic arterial hypotension was maintained. Drinking occurred with a latency of 22 +/- 6 min and 13.2 +/- 1.8 ml H2O/kg was consumed during 2 h of vena caval constriction. Water intake was significantly correlated with the average reduction in blood pressure (r = 0.86; n = 8; P less than 0.01) but not with plasma renin activity. The role of angiotensin II (ANG II) in the drinking and secretion of AVP in response to decreased venous return was evaluated using the ANG II receptor blocker, saralasin, infused intravenously (iv) or intracerebroventricularly (icv). Intravenous, but not icv, infusion of saralasin during vena caval constriction reduced the ability of the dogs to maintain arterial blood pressure (P less than 0.05). However, neither iv nor icv saralasin significantly affected water intake or the rise in plasma AVP in response to vena caval constriction when compared to their respective controls. Taken together, these data show that angiotensin is important in the maintenance of systemic arterial blood pressure but is not essential for the rise in plasma AVP or drinking in response to an acute reduction in venous return. It is suggested that either arterial baroreceptors or "low-pressure" volume receptors or both mediate the drinking and AVP responses in the presence of central blockade of the effects of circulating angiotensin.

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Role of arteria baroreceptor input on thirst and urinary responses to intracerebroventricular angiotensin II

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1993.265.3.r591 ◽

1993 ◽

Vol 265 (3) ◽

pp. R591-R595 ◽

Cited By ~ 4

Author(s):

R. L. Thunhorst ◽

S. J. Lewis ◽

A. K. Johnson

Keyword(s):

Blood Pressure ◽

Angiotensin Ii ◽

Arterial Blood Pressure ◽

Water Intake ◽

Enzyme Inhibitor ◽

Ang Ii ◽

Converting Enzyme ◽

Arterial Blood ◽

Endogenous Formation

Intracerebroventricular (icv) infusion of angiotensin II (ANG II) in rats elicits greater water intake under hypotensive, compared with normotensive, conditions. The present experiments used sinoaortic baroreceptor-denervated (SAD) rats and sham-operated rats to examine if the modulatory effects of arterial blood pressure on water intake in response to icv ANG II are mediated by arterial baroreceptors. Mean arterial blood pressure (MAP) was raised or lowered by intravenous (i.v.) infusions of phenylephrine (1 or 10 micrograms.kg-1 x min-1) or minoxidil (25 micrograms.kg-1 x min-1), respectively. The angiotensin-converting enzyme inhibitor captopril (0.33 mg/min) was infused i.v. to prevent the endogenous formation of ANG II during testing. Urinary excretion of water and solutes was measured throughout. Water intake elicited by icv ANG II was inversely related to changes in MAP. Specifically, rats drank more water in response to icv ANG II when MAP was reduced by minoxidil but drank less water when MAP was elevated by phenylephrine. The influence of changing MAP on the icv ANG II-induced drinking responses was not affected by SAD. These results suggest that the modulatory effects of arterial blood pressure on icv ANG II-induced drinking can occur in the absence of sinoaortic baroreceptor input.

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

AJP Renal Physiology ◽

10.1152/ajprenal.00142.2004 ◽

2005 ◽

Vol 288 (5) ◽

pp. F1044-F1052 ◽

Cited By ~ 18

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.

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Circadian variations of atrial natriuretic peptide in normal people and its relationship to arterial blood pressure, plasma renin activity and aldosterone level

International Journal of Cardiology ◽

10.1016/0167-5273(94)90245-3 ◽

1994 ◽

Vol 46 (3) ◽

pp. 229-233 ◽

Cited By ~ 17

Author(s):

Fu-Tien Chiang ◽

Chuen-Den Tseng ◽

Kwan-Li Hsu ◽

Huey-Ming Lo ◽

Yung-Zu Tseng ◽

...

Keyword(s):

Blood Pressure ◽

Atrial Natriuretic Peptide ◽

Plasma Renin Activity ◽

Arterial Blood Pressure ◽

Natriuretic Peptide ◽

Plasma Renin ◽

Circadian Variations ◽

Aldosterone Level ◽

Arterial Blood ◽

Normal People

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

Clinical Science ◽

10.1042/cs0480147 ◽

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.

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Functional Interaction between Angiotensin and Sympathetic Reflexes in Cats

Clinical Science ◽

10.1042/cs0620051 ◽

1982 ◽

Vol 62 (1) ◽

pp. 51-56 ◽

Cited By ~ 17

Author(s):

R. Hatton ◽

D. P. Clough ◽

S. A. Adigun ◽

J. Conway

Keyword(s):

Blood Pressure ◽

Central Venous Pressure ◽

Arterial Blood Pressure ◽

Venous Pressure ◽

Partial Recovery ◽

Ang Ii ◽

Central Venous ◽

Efferent Nerve ◽

Arterial Blood ◽

Sympathetic Reflexes

1. Lower-body negative pressure (LBNP) was used to stimulate sympathetic reflexes in anaesthetized cats. At −50 mmHg for 10 min it caused transient reduction in central venous pressure and systemic arterial blood pressure. Arterial blood pressure was then restored within 30 s and there was a tachycardia. Central venous pressure showed only partial recovery. The resting level of plasma renin activity (PRA; 2.9–3.2 ng h−1 ml−1) did not change until approximately 5 min into the manoeuvre. 2. When converting-enzyme inhibitor (CEI) was given 75 s after the onset of suction it caused a greater and more sustained fall in arterial blood pressure than when administered alone. The angiotensin II (ANG II) antagonist [Sar1,Ala8]ANG II produced similar effects after a short-lived pressor response. 3. This prolonged fall in arterial blood pressure produced by CEI was not associated with reduced sympathetic efferent nerve activity. This indicates that the inhibitor affects one of the peripheral actions of angiotensin and in so doing produces vasodilatation of neurogenic origin. 4. These findings suggest that angiotensin, at a level which does not exert a direct vasoconstrictor action, interacts with the sympathetic nervous system to maintain arterial blood pressure when homeostatic reflexes are activated. A reduction in the efficiency of these reflexes by CEI may contribute to its hypotensive effect.

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

Acta Endocrinologica ◽

10.1530/acta.0.1190257 ◽

1988 ◽

Vol 119 (2) ◽

pp. 257-262 ◽

Cited By ~ 1

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.

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Augmentation of respiratory sinus arrhythmia in response to progressive hypercapnia in conscious dogs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2001.280.5.h2336 ◽

2001 ◽

Vol 280 (5) ◽

pp. H2336-H2341 ◽

Cited By ~ 18

Author(s):

Fumihiko Yasuma ◽

Jun-Ichiro Hayano

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Arterial Blood Pressure ◽

Respiratory Sinus Arrhythmia ◽

Physiological Response ◽

Minute Ventilation ◽

Control Level ◽

Conscious Dogs ◽

Sinus Arrhythmia ◽

Arterial Blood

Respiratory sinus arrhythmia (RSA) may serve to enhance pulmonary gas exchange efficiency by matching pulmonary blood flow with lung volume within each respiratory cycle. We examined the hypothesis that RSA is augmented as an active physiological response to hypercapnia. We measured electrocardiograms and arterial blood pressure during progressive hypercapnia in conscious dogs that were prepared with a permanent tracheostomy and an implanted blood pressure telemetry unit. The intensity of RSA was assessed continuously as the amplitude of respiratory fluctuation of heart rate using complex demodulation. In a total of 39 runs of hypercapnia in 3 dogs, RSA increased by 38 and 43% of the control level when minute ventilation reached 10 and 15 l/min, respectively ( P < 0.0001 for both), and heart rate and mean arterial pressure showed no significant change. The increases in RSA were significant even after adjustment for the effects of increased tidal volume, respiratory rate, and respiratory fluctuation of arterial blood pressure ( P < 0.001). These observations indicate that increased RSA during hypercapnia is not the consequence of altered autonomic balance or respiratory patterns and support the hypothesis that RSA is augmented as an active physiological response to hypercapnia.

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