Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The role of arginine-vasopressin in the pathogenesis of malignant deoxycorticosterone (DOC) hypertension of rats was investigated. 2. In rats with malignant DOC hypertension plasma arginine-vasopressin concentrations increased more than tenfold subsequent to volume depletion and a rise of serum osmolality. 3. The injection of a specific antibody serum for arginine-vasopressin caused a marked fall of blood pressure in rats with malignant DOC hypertension, whereas the injection of angiotensin II antiserum did not affect blood pressure. 4. In rats exhibiting a benign course of DOC hypertension plasma concentrations of arginine-vasopressin were increased threefold in comparison with normotensive control rats; the injection of an arginine-vasopressin antiserum induced a significant but small fall of blood pressure. 5. It is concluded that in the pathogenesis of malignant DOC hypertension arginine-vasopressin might play the role that the renin-angiotensin system plays in the pathogenesis of malignant renal hypertension.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Vasopressin and malignant deoxycorticosterone hypertension in rats. 107 63

1. The blood-bathed organ technique was employed to study the effects of angiotensin II and catecholamines on an isolated everted rat aorta bathed in the extracorporeal circulating blood of adult dogs and cats. 2. When the injections were made into the bathing blood close to the everted rat aorta, angiotensin II was half as potent as adrenaline or noradrenaline on a molar basis. 3. After intravenous injections, the vasoconstrictor potency of angiotensin was twenty times that of adrenaline or noradrenaline on the everted rat aorta. The increase in potency was due to the interaction of angiotensin II with catecholamines on the preparation. 4. Intravenous phenoxybenzamine abolished the potentiated vasoconstrictor effect of angiotensin II on the blood-bathed everted rat aorta, but it did not abolish the pressor effect of angiotensin II on the cardiovascular system of the animals. The results suggest that catecholamines released into the circulating blood by intravenous angiotensin II do not play an important role in the pressor effect of angiotensin II.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Interaction of angiotensin II with catecholamines in the circulation of the dog and cat. 107 64

1. Labetalol, a compound with both alpha- and beta-adrenoreceptor-blocking actions, was given intravenously (1-5-2-0 mg/kg) in twenty recumbent hypertensive patients. 2. There was a rapid reduction in systolic and diastolic pressures in all, maintained up to 24 h in some subjects. 3. Severe hypotension was not seen in recumbent subjects, but postural hypotension was common. 4. Labetalol caused significant lowering of heart rate. 5. Labetalol induced significant and related lowering of plasma angiotensin II and aldosterone concentrations, most obviously when these were initially high. 6. In a cross-over comparison in five patients against 10 mg of propranolol intravenously, labetalol was more effective in lowering blood pressure, but less effective in lowering pulse rate or plasma angiotensin II.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Effects of intravenous labetalol on blood pressure, angiotensin II and aldosterone in hypertension: comparison with propranolol. 107 71

1. Hindlimb vascular resistance (HVR) was measured before and after pharmacological autonomic blockade in unanesthetized renal cellophan-wrap hypertensive or normotensive rabbits with previously implanted Doppler ultrasonic flowmeters. 2. When the blood pressure was restored to resting values after autonomic block, the elevated resting HVR in the hypertensive rabbits was entirely accounted for by an increased non-autonomic component (i.e. HVR after block). If the pressure was not restored after block the autonomic component (i.e. resting HVR minus non-autonomic HVR) was overestimated and the non-autonomic component was underestimated. 3. During maximum vasodilatation the minimum HVR was significantly higher in the hypertensive rabbits than in the normotensive group, probably due to structural differences of resistance vessels. 4. Reactivity of the hindlimb bed to noradrenaline, angiotensin II and vasopressin injections was approximately twice as great in the hypertensive rabbits as in the sham-operated group, probably as a consequence of the structural changes.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Assessment of autonomic and non-autonomic components of resting hindlimb vascular resistance and reactivity to pressor substances in renal hypertensive rabbits. 107 82

1. Competitive or non-competitive inhibition of the myotropic and pressor response of angiotensin II is dependent on the nature of the substituent in position 8 of the antagonist peptide analogue. Substituents in other positions of the molecule, particularly position 1, contribute greatly to the potency of these antagonists. 2. As is evidenced after adrenalectomy or after blockade with phentolamine and phenoxybenzamine, the initial pressor activity observed with all the antagonistic peptides is partially due to the release of catecholamines and partially to a direct myotropic effect. 3. [Sar1, Thr8]angiotensin II has been found to possess the lowest agonist to antagonist ratio of all antagonists tested. 4. [Des-Asp1, Ile8]angiotensin II selectively and specifically inhibits the release of aldosterone from adrenal cortex. Thus, unlike angiotensin II, this heptapeptide has pronounced organ specificity, suggesting that the heptapeptide (angiotensin III) is the aldosterone-releasing hormone.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Inhibition of the pressor and aldosterone-releasing effects of angiotensin II. 107 65

1. The angiotensin II antagonism by newly synthesized 8-C-phenylglycine analogues of [5-isoleucine]angiotensin II in different preparations was investigated in vitro and in vivo. 2. All analogues competitively inhibited the myotropic effect of angiotensin II on the isolated colon ascendens of the guinea-pig and the stomach of the rat. 3. In normotensive dogs, cats, rabbits, guinea-pigs and rats the blood pressure response to infused angiotensin II was inhibited by the antagonists. The angiotensin II-induced fall in renal blood flow in the dog was blocked during infusion of the analogues. Acute renal hypertension in rats was significantly decreased. Of conscious rats variously with normal blood pressures, spontaneous hypertension and chronic renal hypertension, only in the last group could a marked uniform fall in blood pressure be demonstrated. The central pressor effect of angiotensin II was also inhibited in conscious rats. 4. 8-C-Phenylglycine analogues of [5-isoleucine]-angiotensin II exhibit a specific antagonistic activity to endogenous and exogenous angiotensin II.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Comparative pharmacology of new specific angiotensin antagonists. 107 69

1. Experiments were carried out on two groups of anaesthetized greyhounds. The response of the first group to infusions of angiotensin II into a vertebral artery for 5 min and to bilateral occlusion of the common carotid arteries for 2 min was studied before and after bilateral ablation of the areas postrema. The response of the second group to infusions of angiotensin and to carotid occlusion was studied before and after mid-collicular transection of the midbrain. 2. Bilateral ablation of the areas postrema abolished the response to angiotensin infused into a vertebral artery at the dose used but did not significantly alter the response to carotid occlusion. Transection of the midbrain did not abolish the response to either procedure. 3. It is concluded that the structures involved in the cardiovascular response to carotid occlusion are anatomically distinct from the area postrema and that neither response requires the integrity of connections above the pons. 4. An attempt has been made to construct a schematic diagram of the vasomotor centre.
Clin Sci Mol Med Suppl 1975 Jun
PMID:The vasomotor centre and its afferent pathways. 107 71

1. Antibodies against angiotensin II were purified by affinity chromatography. 2. When injected intravenously into rats, the antibody distributed in the extracellular space with a half-time of 11 h and a distribution volume of about 10 ml/100 g body weight. The antibody was eliminated with a half-time of 7 days. 3. Plasma angiotensin II concentrations increased about 100-fold the control values 7 min after antibody injection and declined in parallel with the antibody concentration. It was calculated that only about 1--4% of the binding capacity of the antibody was occupied by angiotensin throughout the experiment. 4. Since the plasma renin concentration was normal, except during the short initial phase of stimulation, it is concluded that upon antibody injection the renin-angiotensin system rapidly reached an equilibrium, with concentrations of free angiotensin close to or identical with normal concentrations.
Clin Sci Mol Med Suppl 1975 Jun
PMID:The response of the renin--angiotensin systems in rats to the injection of angiotensin II antibodies. 107 76

1. Inhibition of prostaglandin synthesis by indomethacin induced an increase in blood pressure which did not occur when rats were bilaterally nephrectomized. 2. The blood pressure effect was related to the state of sodium balance and thus to the activity of the renin--angiotensin system. 3. Indomethacin induced a decrease in renal blood flow. 4. Angiotensin receptor blockade with Sar1-Ala8-angiotensin II blunted the blood pressure effect and prevented the renal haemodynamic changes induced by indomethacin.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Effect of a competitive angiotensin antagonist on the renal haemodynamic changes induced by inhibition of prostaglandin synthesis in rats. 107 81

1. In rabbits actively immunized against angiotensin II (AII), the appearance of anti-AII antibodies was associated with a rise in plasma renin activity (PRA), which did not occur in mock-immunized controls. 2. In conscious rabbits, infusion of the angiotensin inhibitor, Sar1-Ala8-angiotensin II (P-113), at rates of 0.055, 0.22 or 1.1 nmol min-1 kg-1 into the renal artery, caused dose-related increases in arterial PRA and renal arteriovenous PRA difference. Renal blood flow fell with the high dose, but not with the low or medium doses. A fall in arterial pressure, asynchronous with peak renin secretion, accompanied the medium- and high-dose infusions. 3. Intravenous infusion of inhibitor P-113, 5.5 nmol min-1 kg-1, into anaesthetized rats produced highly significant increases in PRA and plasma renin concentration without reduction in arterial pressure. There were no changes in PRA or plasma renin concentration in saline-infused control rats. 4. These findings suggest that AII blockade interrupts a negative feedback loop controlling renin secretion.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Angiotensin blockade in studies of the feedback control of renin release in rats and rabbits. 107 86


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