Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In conscious dogs, we examined the hypothesis that the effects of atrial natriuretic peptide (ANP) are mediated by cyclic GMP and tested whether stimulation of the intracellular pathway beyond the ANP receptor level still exerts ANP-like effects during tolerance to ANP in heart failure. We studied the hemodynamic, renal, and hormonal effects of the cyclic GMP analogue 8-bromo-cyclic GMP (8-Br-cyclic GMP) in conscious dogs before and after induction of congestive heart failure by right ventricular pacing. In healthy dogs, 8-Br-cyclic GMP (1-100 micrograms/kg/min) dose-dependently decreased mean arterial pressure (MAP -19% by 100 micrograms/kg/min) and total peripheral resistance (TPR -22%) with no change in cardiac output (CO) and right atrial pressure, increased urine flow (UF 52%), and sodium excretion (UNaV 135%). Plasma renin (62%) and norepinephrine (NE 24%) were increased. In dogs with heart failure, 8-Br-cyclic GMP induced a similar arteriolar dilation (MAP -16%, TPR -23%) with no change in CO and preload. However, the effects on renal excretory function were abolished or markedly attenuated (UF -4%, UNaV 7%). Plasma renin (163%) and aldosterone (40%) were increased. Our findings support the hypothesis that the renal effects of ANP are mediated by cyclic GMP in vivo. The attenuation of renal effects of 8-Br-cyclic GMP in heart failure does not prove but is in agreement with the hypothesis that an intracellular defect beyond cyclic GMP production might be involved in the tolerance to ANP in heart failure.
 ...
PMID:Hemodynamic, renal, and hormonal effects of 8-Br-cyclic GMP in conscious dogs with and without congestive heart failure. 247 97

The early blood pressure and hemodynamic effects of the converting enzyme inhibitor (CEI), captopril, were compared in 23 hypertensive patients with those of a specific angiotensin II antagonist (AA), [Sar1, Thr8] A II. AA reduced mean arterial pressure (MAP) greater than 10 mm Hg only in seven of 23 patients vs 15 of 23 who responded to CEI (p less than 0.02). With both drugs, changes in MAP were not associated with significant changes in cardiac output (p greater than 0.10 for both drugs), but correlated with changes in systemic resistance (TPR); r = 0.84, p less than 0.001 for AA and r = 0.71, p less than 0.001 for CEI. Changes in TPR and MAP correlated significantly and inversely with log plasma renin activity in both instances; for AA, r = 0.829 and for CEI, r = -0.737; p less than 0.001 for both. The slopes of the two regression lines were not significantly different but the intercepts were +8.47 mm Hg for AA vs -10.17 mm Hg for CEI (p less than 0.001). This quantitative difference in response could be attributed either to an agonistic effect of [Sar1, Thr8] A II or to an additional vasodilator effect of captopril.
 ...
PMID:Constrasts and similarities of acute hemodynamic responses to specific antagonism of angiotensin II ([Sar1, Thr8] A II) and to inhibition of converting enzyme (captopril). 698 75

1. Hypertension secondary to renal disease was studied in non-pregnant and pregnant ewes to determine whether there were any changes in arterial pressure and the distribution of cardiac output and, in particular, whether uteroplacental blood flow was affected. 2. In six non-pregnant, chronically catheterized, uninephrectomized ewes, a reduction in renal blood flow (RBF) to 40-50% of control caused hypertension within 3 h. This was maintained for as long as RBF was reduced (72 h) and returned to control 24 h after the occluder around the renal artery was released. When this experiment was repeated in 16 uninephrectomized pregnant ewes (118-134 days gestation) hypertension occurred within 3 h and was sustained for as long as RBF was reduced (between 24 and 72 h). Arterial pressure returned to control within 24-72 h of restoring RBF. 3. Compared with non-pregnant ewes, pregnant ewes had similar arterial pressures, higher cardiac outputs (CO; P < 0.001) and heart rates (HR; P < 0.001), lower total peripheral resistances (TPR; P < 0.001) and similar blood flows to brain, ovary, pancreas, kidney and spleen. Splenic vascular resistance (VR) was greater (P = 0.006), gut blood flow was greater (P < 0.05) and gut VR was less (P < 0.05). Myoendometrial blood flow/g was greater (P < 0.005) and myoendometrial VR was less (P = 0.006). 4. In pregnant sheep with renal clip hypertension, there was no change in CO and HR, but TPR increased (P < 0.01), as did plasma renin activity. Gut, brain, pancreatic and myoendometrial VR were increased as long as RBF was reduced; in addition, myoendometrial VR remained high for the rest of the experiment. Placental blood flow was unchanged at 3 h; 24-72 h later it was reduced (P < 0.05) and remained low. Placental VR was increased 24-72 h after RBF was restored when ewes were again normotensive. 5. Thus, one-clip, one-kidney renal hypertension in the pregnant ewe was due to increased TPR associated with a fall in uteroplacental blood flow that persisted even when RBF was restored and ewes were normotensive. This reduction in uteroplacental blood flow could account for the high foetal morbidity and mortality that occurs in pregnant women with renovascular hypertension.
 ...
PMID:Effects of one-clip, one-kidney hypertension in chronically catheterized pregnant ewes. 914 84

1. Eight healthy subjects were investigated on four occasions at least 1 week apart when they either ate a standard 3100 kJ cold meal or fasted. One hour earlier, either 50 mg atenolol or placebo was administered. 2. Eating was followed by prominent changes of systolic cardiovascular function: a rise of heart rate (+7, 95% CI: 4 to 9 beats min(-1)), systolic BP (+5, CI: 1 to 8 mmHg), a drop of diastolic BP (-6, CI:-9 to -3 mmHg), shortening of the pre-ejection period PEP (-11, CI: -13 to -9 ms) and electromechanical systole QS2c (-13, CI: -17 to -8 ms), a rise of the estimated cardiac output CO (+1.3, CI: 1.0 to 1.6 1 min(-1)) and a reduction of the calculated total peripheral resistance TPR (-306, CI: -389 to -222 dyn s cm(-5)). 3. Eating was also followed by an increase of the non-renal clearance of sorbitol (as a measure of hepatic blood flow) and this change was larger than proportional to the increase of CO. The plasma renin activity rose after the meal but the venous plasma noradrenaline and adrenaline concentrations were not affected. 4. The postprandial effects peaked over the first 1-2 h after the meal but remained well detectable up to 4 h after eating. 5. The administration of 50 mg atenolol before the meal reduced the postprandial effects to the same extent as the atenolol effects in the fasting state. This lack of interaction (or mere arithmetic additivity) indicates that the efferent beta1-adrenergic tone does not play a predominant role in the modulation of postprandial cardiovascular changes.
 ...
PMID:Cardiovascular effects of eating, atenolol and their interaction: beta1-adrenergic modulation does not play a predominant role in the genesis of postprandial effects. 1295 90

The purpose of the present study was to quantify the antihypertensive effect of the total flavonoid (TF), extracted from the seed of Astragalus complanatus R. Brown, and to observe its effect on the renin-angiotensin system (RAS) in both renal hypertensive rats (RHR) and spontaneously hypertensive rats (SHR). RHR were created by the two-kidney one clip (2K1C) method. Systolic blood pressure was measured in conscious rats by the tail-cuff method. Plasma angiotensin II (AngII) and plasma renin activity (PRA) were measured with radioimmunoassay at 60 min after drug administration. The effects of TF on cardiac hemodynamics were also recorded in anesthetized RHR and SHR. TF was given by oral administration in low dose (100 mg/kg) and high dose (200 mg/kg) respectively. Compared to pre-administration control, TF induced an obvious decrease in systolic blood pressure in conscious normotensive Wistar rat, RHR and SHR. In the three groups the systolic blood pressure reached the lowest value at 60 min after TF. TF also induced a significant decrease in blood pressure in anesthetized RHR and SHR. At 60 min after treatment of TF, mean arterial pressure in high dose group (200 mg/kg) was decreased by 17% in RHR and by 17% in SHR respectively (P < 0.01). The depressor effect of TF lasted for at least 60 min. Cardiac output, heart rate and +/- dp/dtmax did not change. Conversely, total peripheral resistance was significantly decreased. The decrease in plasma AngII was found in both RHR and SHR. On the contrary, PRA increased at the same time. These findings suggested that TF is effective in reducing blood pressure in both RHR and SHR. The antihypertensive action of TF was attributed to a decrease in TPR secondary to a decrease in plasma concentration of AngII caused by TF.
 ...
PMID:Antihypertensive effect of total flavonoid fraction of Astragalus complanatus in hypertensive rats. 1620 55

Both intensive training and bed confinement impair orthostatic tolerance, however, moderate training may exert beneficial effect on cardiovascular adjustment to gravitational stimuli. It was hypothesized that moderate training attenuates effects of bed rest. To test this assumption 24 healthy male volunteers aged 20.8+/-0.9 yrs were subjected to 6 degrees head down bed rest (HDBR) for 3 days before and after 6 weeks of moderate endurance training. Before and after HDBR graded LBNP tests (-15, -30, -50 mmHg) were performed. During these tests heart rate (HR), stroke volume (SV), blood pressure (BP), plasma catecholamines, ACTH, adrenomedullin, atrial natriuretic peptide, plasma renin activity (PRA) and hematocrit were determined. HDBR did not systematically influence LBNP tolerance up to -50 mmHg, but it enhanced rates of reduction of SV, cardiac output and systolic BP and increased elevations of HR and PRA. Training did not alter significantly effects of HDBR on LBNP-induced changes in HR, SV, CO and TPR but it attenuated decrease in systolic BP and diminished increases in plasma noradrenaline and PRA. In conclusion, training has negligible effect on the HDBR-induced changes in central hemodynamics during LBNP but may increase vascular sensitivity to some vasoconstricting factors.
 ...
PMID:Cardiovascular and neurohormonal responses to lower body negative pressure (LBNP): effect of training and 3 day bed rest. 1724 93