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

The pathophysiological role of an increase in circulating vasopressin in sustaining global and regional vasoconstriction in patients with congestive heart failure has not been established, particularly in patients with hyponatraemia. To assess this further, 20 patients with congestive heart failure refractory to digoxin and diuretics were studied before and 60 minutes after the intravenous injection (5 micrograms/kg) of the vascular antagonist of vasopressin [1(beta-mercapto-beta,beta-cyclopentamethylene-propionic acid), 2-(0-methyl) tyrosine] arginine vasopressin. Ten patients were hyponatraemic (plasma sodium less than 135 mmol/l) and 10 were normonatraemic. In both groups of patients the vascular vasopressin antagonist did not alter systemic or pulmonary artery pressures, right atrial pressure, pulmonary capillary wedge pressure, cardiac index, or vascular resistances. Furthermore, there was no change in skin and hepatic blood flow in either group after the injection of the vascular antagonist. Only one patient in the hyponatraemic group showed considerable haemodynamic improvement. He had severe congestive heart failure and a high concentration of plasma vasopressin (51 pmol/l). Plasma renin activity, vasopressin, or catecholamine concentrations were not significantly changed in response to the administration of the vasopressin antagonist in either the hyponatraemic or the normonatraemic groups. Patients with hyponatraemia, however, had higher baseline plasma catecholamine concentrations, heart rate, pulmonary pressure and resistance, and lower hepatic blood flow than patients without hyponatraemia. Plasma vasopressin and plasma renin activity were slightly, though not significantly, higher in the hyponatraemic group. Thus the role of vasopressin in sustaining regional or global vasoconstriction seems limited in patients with congestive heart failure whether or not concomitant hyponatraemia is present. Vasopressin significantly increases the vascular tone only in rare patients with severe congestive heart failure and considerably increased vasopressin concentrations. Patients with hyponatraemia do, however, have raised baseline catecholamine concentrations, heart rate, pulmonary arterial pressure and resistance, and decreased hepatic blood flow.
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PMID:Hormonal, global, and regional haemodynamic responses to a vascular antagonist of vasopressin in patients with congestive heart failure with and without hyponatraemia. 379 Mar 79

This is a review of the literature concerning current views of renal physiology. Types and functions of nephrons, the morphology of the loop of Henle, and the function of renal enzymes are discussed. Vasopressin serves the main function of conserving water in the body. The renin-angiotensin-aldosterone system regulates sodium excretion. The sympathetic vasomotor nerves prevent the loss of both sodium and water. These 3 factors operate by changing the proportion of superficial cortical to deep juxta-medullary nephrons functioning in the kidney at any time. The shift from superficial to deep nephrons prevents excess salt and water loss from the body through the urine.
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PMID:The vogue in renal physiology: a review article. 431 23

1. Mucosal water and sodium transfer were measured in everted sacs of rat jejunum.2. Rats maintained on a high sodium diet did not show consistently reduced mucosal water transfer and aldosterone also failed to stimulate transfer unless the control untreated values were low.3. Adrenalectomy produced little reduction in mucosal water transfer and aldosterone was without effect on water transfer in sacs from adrenalectomized rats.4. Vasopressin had no effect on mucosal transfer.5. Levels of water transfer were not reduced after hypophysectomy nor did aldosterone injection increase transfer.6. Mucosal water transfer in sacs from adrenalectomized-nephrectomized rats was low and was significantly increased by aldosterone injection or by injection of crude kidney extract.7. A significant increased mucosal water and sodium transfer was observed when sacs from adrenalectomized-nephrectomized rats were incubated with angiotensin at a concentration of 10(-10)g/ml.8. It is suggested that the renin-angiotensin system may be involved in the maintenance of sodium homoeostasis by a direct action on sodium transporting mechanisms.
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PMID:The effect of the renin-angiotensin system on mucosal water and sodium transfer in everted sacs of rat jejunum. 432 43

1. The rabbit rectum superfused with blood or Krebs solution was used to assay vasopressin in circulating blood and in plasma extracts respectively.2. Vasopressin was released by a rapid fall in diastolic pressure of as little as 5 mmHg, and the amount of vasopressin released was proportional to the magnitude of the fall in diastolic pressure in the range studied. These results would indicate that vasopressin release follows the magnitude of the fall in diastolic pressure more closely than the actual decrease in blood volume in haemorrhagic hypotension.3. It was shown that the time required to induce an increase in circulating vasopressin is inversely proportional to the severity of the fall in diastolic pressure; this suggested that the stimulation of neurosecretory reflex arc varies with the intensity of the stimulus.4. The slight changes in plasma renin activity as well as the pattern of renin release suggested the unlikeliness of the influence of renin upon vasopressin secretion under these circumstances. On the contrary, the results suggested that the secretion of large amounts of vasopressin tended to inhibit renin release.
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PMID:Changes in plasma levels of vasopressin and renin in response to haemorrhage in dogs. 472 45

We have investigated the relative importance of angiotensin and vasopressin in the regulation of arterial pressure following permanent interruption of supraspinal sympathetic influences. To accomplish this aim, the spinal cord of 12 dogs was transected just above the intervertebral foramen of C-6; several days later, we gave first a potent blocker of the vasculotropic actions of vasopressin and 40 min later captopril. The same experiment was performed in other dogs with the drug order reversed. Mean arterial pressure and heart rate were recorded continuously and blood samples were taken to measure plasma renin activity and plasma catecholamines. All studies were carried out at three levels of hydration: normal, after 36 h water deprivation and following an overnight infusion of 0.9% saline. Conscious dogs with complete surgical sympathectomy by spinal cord section had normal mean arterial pressure, heart rate and plasma renin activity but undetectable levels of catecholamines. Captopril produced significant falls in mean arterial pressure that were greatest in water deprivation and least in volume loading, whether the drug was given before or after treatment with the vasopressin antagonist. On the other hand, the vasopressin antagonist modified mean arterial pressure only in the water deprived state. In spinal dogs the renin angiotensin system assumes a primary role in maintaining normal mean arterial pressure at various extremes of body fluid volumes. Vasopressin plays a role only after removal of the two dominant systems.
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PMID:Hierarchy of blood pressure control mechanisms after spinal sympathectomy. 640 Jan 21

To assess in vivo functional interactions of vasopressor substances, norepinephrine and vasopressin, with renal prostaglandins and kallikrein-kinin system which are responsible for the vasodepressor mechanism in the kidney, we evaluated chronic effects of norepinephrine (1.8 mg/kg/day ip) and vasopressin (7.2 U/kg/day ip) on urinary prostaglandin E excretion and urinary kallikrein excretion in conscious rats. Both norepinephrine and vasopressin induced a sustained increase in systolic blood pressure. Norepinephrine induced slight but significant increases in urinary prostaglandin E excretion and urinary kallikrein excretion which were sustained for up to 6 days. Vasopressin induced a marked increase in urinary prostaglandin E excretion which was sustained for up to 6 days, whereas it induced a sustained decrease in urinary kallikrein excretion. Circulating angiotensin II levels was not changed by norepinephrine, but was decreased by vasopressin. These results indicate that renal prostaglandin E may not correlate with renal kallikrein-kinin and renin-angiotensin system in the responses to norepinephrine and vasopressin, and that vasopressin may be a more potent stimulator of the synthesis or release of renal prostaglandin E.
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PMID:Chronic effects of norepinephrine and vasopressin on urinary prostaglandin E and kallikrein excretions in conscious rats. 656 34

1. Vasopressin deficient homozygous Brattleboro rats develop malignant renal hypertension following complete aortic-ligature between the renal arteries. 2. This form of hypertension is associated with high plasma renin activity (PRA) and plasma angiotensin II (AII) levels and a high incidence of the specific vascular lesions of fibrinoid necrosis in both Brattleboro and Long-Evans rats. 3. The levels of PRA and AII in the malignant hypertensive Brattleboro rats were not different from those in Long-Evans rats with malignant hypertension. 4. No compensation by the renin-angiotensin system therefore could be demonstrated for the lack of vasopressin in malignant hypertensive Brattleboro rats. 5. Vasopressin does not appear to be essential as a pressor hormone in the development of malignant renal hypertension and fibrinoid can occur in the absence of vasopressin.
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PMID:Vascular lesions and angiotensin in malignant hypertension in the absence of vasopressin. 675 78

Plasma vasopressin concentration (PAVP), renal function, and effectors of vasopressin release were evaluated in male volunteers during running at heart rates of 0, 35, 70, and 100% of maximum after 10 h abstinence from water (normal hydration) and at 100% after ingestion of 300 ml water. Plasma renin activity (PRA) and PAVP were linearly correlated and correlated to work intensity over all observations. Changes in PAVP were not correlated with changes in plasma osmolality (POSMOL) and plasma volume (PV) over all observations. Furthermore, despite similar changes in POSMOL, PV, PRA, body weight, mean arterial pressure, and plasma lactate concentration, the increase in PAVP after maximal exercise was greater during normal hydration than the water-supplemented state. Decreased urine flow observed in association with exercise was characterized by increased free water and decreased osmotic and creatinine clearances. Thus increased PAVP associated with exercise appears not to play a role in the concomitant antidiuresis. Vasopressin stimuli are probably variable at different times during exercise and may include factors other than those measured.
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PMID:Plasma renin activity, vasopressin concentration, and urinary excretory responses to exercise in men. 700 89

To determine if the subnormal blood pressure recovery after hemorrhage in Brattleboro rats is due to secondary abnormalities in the renin-angiotensin or sympathetic nervous systems, we measured the hemodynamic, catecholamine, and renin activity responses to moderate acute hemorrhage in anesthetized Brattleboro rats. Results were compared to responses in groups of animals matched for either age or weight. Blood pressure recovery was significantly blunted (P less than 0.01) in Brattleboro rats compared to that in either control group, but heart rate responses were similar. Basal plasma norepinephrine was significantly higher in Brattleboro rats than in controls (P less than 0.001), but the response to hemorrhage was not significantly different. Both plasma epinephrine levels and renin activity were significantly higher before hemorrhage and increased more after hemorrhage in vasopressin-deficient animals. Plasma vasopressin in controls increased approximately 10-fold, reaching levels of 790 +/- 140 pg/ml in age-matched controls and 425 +/- 60 pg/ml in weight-matched controls. Vasopressin levels in Brattleboro rats were undetectable both before and after hemorrhage. We conclude from these data that the subnormal blood pressure recovery observed in vasopressin-deficient rats is not due to secondary abnormalities of the renin-angiotensin or sympathetic nervous systems, but, instead, is related more directly to the vasopressin deficiency.
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PMID:Cardiovascular, sympathetic, and renin-angiotensin system responses to hemorrhage in vasopressin-deficient rats. 704 52

The role of brain angiotensin II (ANG II) in mediating cardiovascular, vasopressin, and renin responses to hemorrhage was assessed in conscious spontaneously hypertensive rats (SHR) and in normotensive Wistar-Kyoto (WKY) and Wistar rats. Intracerebroventricular administration of losartan (10 micrograms) and saralasin (1 microgram.microliter-1.min-1) produced a markedly greater fall in blood pressure and a reduced tachycardia during and after hemorrhage (15 ml/kg) compared with the artificial cerebrospinal fluid control in SHR and Wistar rats but not in WKY rats. Vasopressin release after hemorrhage was also impaired, but renin release was enhanced by intracerebroventricular ANG II antagonists in SHR and Wistar rats but not in WKY rats. Losartan and saralasin produced remarkably similar effects on the cardiovascular, vasopressin, and renin responses to hemorrhage. These data suggest that brain ANG II acting through AT1 receptors plays an important physiological role in mediating rapid cardiovascular regulation and vasopressin release in response to hemorrhage. The relative importance of brain angiotensin system may vary in different strains of rate.
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PMID:Central ANG II-receptor antagonists impair cardiovascular and vasopressin response to hemorrhage in rats. 761 27


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