Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to examine the hemodynamic, renal, and endocrine effects of exogenous human atrial natriuretic factor (ANF), together with its pharmacokinetics, in healthy volunteers. Ten subjects participated in this study, in which the effects of a single bolus dose of ANF and of a matched vehicle injection were compared under a 135 mmol/day sodium intake. Doses of 3, 12.5, and 25 micrograms of ANF were given to 1 subject each, and doses of 50 and 100 micrograms were given to 4 and 3 subjects, respectively. Significantly, hemodynamic changes occurred at the 100 micrograms dose, when mean blood pressure decreased by 15% and heart rate increased reciprocally. Diuresis and natriuresis tended to increase following 50 micrograms but increased significantly and in a prolonged fashion following 100 micrograms of ANF. Atrial natriuretic factor did not cause significant changes in plasma catecholamine, renin activity, and aldosterone levels at any dose, although aldosterone tended to decrease. Plasma arginine-vasopressin concentrations decreased significantly following 100 micrograms. Plasma cyclic GMP levels increased in all subjects and in a dose-dependent fashion. Plasma ANF concentrations peaked 3-5 min following the bolus injection and returned toward baseline values within 10-60 min. Although with doses of less than or equal to 50 micrograms plasma ANF levels increased up to 8 to 50-fold, compared to baseline values, the only significant change was the increase in plasma cyclic GMP levels, perhaps because the effects of ANF were successfully masked by counter-regulatory mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1988 Jun
PMID:Effects and pharmacokinetics of bolus injections of atrial natriuretic factor in normal volunteers. 245 57

Pressor response to graded infusion of angiotensin II, noradrenaline, arginine-vasopressin, and serotonin and blood pressure change following indomethacin, an inhibitor of cyclooxygenase, were examined in conscious sheep, before and during the development of cyclosporin A-induced hypertension. Cyclosporin caused an increase in mean blood pressure from 68 +/- 2 to 82 +/- 3 mm Hg (p less than 0.001) and in heart rate from 67 +/- 4 to 91 +/- 4 beats/min (p less than 0.001). Pressor and heart rate responses to all substances tested were not changed by cyclosporin treatment suggesting that changes in pressor responsiveness are unlikely to be involved in the development of cyclosporin hypertension in sheep.
J Cardiovasc Pharmacol 1988 Jun
PMID:Cyclosporin A and pressor responsiveness in sheep. 245 62

To determine whether hypothyroidism alters responsiveness to centrally infused thyrotropin-releasing hormone (TRH), blood pressure and sympathetic nerve responses to various stimuli were recorded in urethane-anesthetized rats. Four weeks after thyroidectomy or treatment with propylthiouracil, pressor responses elicited by intracerebroventricular- (ICV)-infused TRH or by electrical stimulation of the posterior or ventromedial hypothalamus were always accompanied by increased sympathetic nerve activity in all rats. When serum thyroxine levels were lowered in hypothyroid rats, pressor responses to most stimuli, including intravenous injections of norepinephrine, angiotensin, and vasopressin, were inhibited, indicating that peripheral pressor responsiveness had been reduced. For centrally acting stimuli, pressor inhibition was also considered partly caused by a selective decrease in sympathetic vasomotor tone because sympathetic excitation was reduced only during ICV infusions of TRH, but not during posterior hypothalamic stimulation. On the other hand, there was no obvious explanation why both pressor and sympathetic responses to ventromedial hypothalamic stimulation were spared from inhibition. Because sympathetic nerve responses to ICV-infused TRH were reduced by thyroid suppression, these results imply that sympathetic activation by TRH in intact rats is mediated, at least in part, indirectly by way of TRH stimulation of thyroid activity.
J Cardiovasc Pharmacol 1988 Jul
PMID:Selective suppression of pressor and sympathetic responses to centrally infused TRH in hypothyroid rats. 245 34

The present study examined the effects of central and peripheral administration of a vascular (V1) vasopressin (AVP) receptor antagonist on blood pressure, heart rate, and AVP levels in conscious rats. Rats subjected to rapid arterial haemorrhage were administered the AVP V1 antagonist [d(CH2)5Tyr(Me)AVP] either 5 min pre- or 20 min posthaemorrhage. Mean arterial blood pressure (MAP) was monitored for 45 min, after which the animals were killed and selected brain regions and plasma taken for AVP measurement. Intravenous (i.v.) administration of d(CH2)5Tyr(Me)AVP at 10 micrograms kg-1, but not 100 ng kg-1, significantly reduced MAP between 20 and 45 min posthaemorrhage compared with saline-treated controls. In contrast, administration of d(CH2)5Tyr(Me)AVP at 100 ng kg-1 intracerebroventricularly caused an attenuated MAP recovery to haemorrhage comparable with the effect of the antagonist at 10 micrograms kg-1 i.v. Haemorrhage caused a marked increase in circulating AVP levels, which was further enhanced in rats treated with the V1 antagonist at 10 micrograms kg-1 i.v., but no change in AVP levels of selected brain regions. The results indicate a role for AVP in MAP recovery following haemorrhage which may be centrally mediated.
J Cardiovasc Pharmacol 1988 Oct
PMID:Central and systemic effects of a vasopressin V1 antagonist on MAP recovery after haemorrhage in rats. 246 40

Atrial natriuretic peptides (ANP) exert vasodilating and natriuretic actions. The present study was undertaken to test the effect of low dose infusions of synthetic ANP on hemodynamic and humoral variables of patients with severe heart failure. Eight patients, aged 26 to 71 years, with severe congestive heart failure due to ischemic heart disease or idiopathic dilated cardiomyopathy were included in the study. Synthetic human (3-28) ANP was infused at doses ranging from 0.5 to 2 micrograms/min for up to 3 h. Pulmonary capillary wedge pressure fell from 24 +/- 1 to 16 +/- 2 mm Hg (mean +/- SEM) (p less than 0.01) and cardiac index tended to rise from 2 +/- 0.2 to 2.3 +/- 0.2 L/min/m2 (NS), while blood pressure and heart rate did not change. One patient experienced a marked drop in pulmonary capillary wedge and arterial blood pressure that necessitated the administration of saline. ANP infusion did not alter plasma renin activity or plasma aldosterone, norepinephrine, or vasopressin levels. It decreased plasma epinephrine levels from 0.472 +/- 0.077 to 0.267 +/- 0.024 nmol/L (p less than 0.05). Plasma ANP levels were markedly elevated in all patients before initiating the infusion. They had no predictive value for the hemodynamic response to exogenous ANP. No correlation was observed between the hemodynamic effects of ANP and those induced by the subsequently administered converting enzyme inhibitor captopril, which seemed to improve cardiac function more consistently.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1988
PMID:Infusion of atrial natriuretic peptide to patients with congestive heart failure. 246 56

We studied the hemodynamic changes produced in conscious, chronically instrumented rabbits during steady-state administration of atrial natriuretic peptide (ANP). We administered synthetic alpha-human ANP intravenously (i.v.) at progressively increasing doses of 1, 2, and 4 micrograms/min, each for 30 min. In different experiments in each rabbit, we determined the effects of the peptide under closed-loop conditions in the intact animal and the "direct" circulatory effects of the peptide after "total" blockade of the autonomic nervous system (TAB) and after combined neurohumoral blockade (NHB), where in addition the vascular effects of vasopressin and angiotensin II were also prevented. In intact rabbits, ANP produced a dose-related reduction in mean arterial pressure (MAP, -3 to -14%), which was entirely due to a fall in cardiac output (CO, -14 to -20%), and there was a small rise in total peripheral resistance (TPR 5-12%). Heart rate remained unchanged. In rabbits subjected to TAB and NHB, all hemodynamic effects of ANP were attenuated. There were dose-related falls in left and right atrial pressures which reached maxima of -3.3 +/- 0.9 and -1.8 +/- 0.2 mm Hg, respectively. There was a reversible rise in hematocrit, probably owing to a shift of approximately 8% in blood volume. These effects occurred mainly through direct actions of the peptide, and there was no evidence of systemic vasodilatation. The magnitude of reflex autonomic effects appeared to be less than expected for the observed fall in MAP, suggesting that ANP also inhibited cardiovascular reflexes.
J Cardiovasc Pharmacol 1989 Feb
PMID:Direct and neurohumoral cardiovascular effects of atrial natriuretic peptide. 246 43

The effects of noradrenaline (NA, 10(-5) M) and [arginine8]vasopressin (AVP, 10(-7) M) on tension in Ca2+-free medium and on membrane potential, and the inhibition of NA- and AVP-induced contractions by isradipine, have been compared in mesenteric resistance vessels (MRVs) from Wistar-Kyoto (WKY) rats. The release of intracellular Ca2+ by AVP contributed significantly less to its tension development than does that by NA. Nonetheless, the concentration-response curves for inhibition by isradipine of NA- and AVP-induced tonic tension were nearly identical. Similarly, these two agonists produced the same degree of membrane depolarization. In addition, both agonists were able to stimulate large contractions in vessels previously depolarized by 80 mM K+. AVP also stimulated 45Ca influx into rat cultured aortic smooth muscle cells. In contrast to the stimulation of 45Ca influx by KCl depolarization, the agonist-stimulated 45Ca influx was insensitive to inhibition by organic Ca2+ antagonists. It is concluded that Ca2+ entry through receptor-operated Ca2+-permeable channels (ROCs) may contribute to agonist-induced activation of rat aortic and MRV smooth muscle.
J Cardiovasc Pharmacol 1988
PMID:Agonist-induced activation of rat mesenteric resistance vessels: comparison between noradrenaline and vasopressin. 246 70

The effects of endothelin-1 (ET-1) on tension and membrane potential in rat isolated mesenteric resistance vessels (MRVs) and on 45Ca influx, 45Ca efflux, inositol-1,4,5-triphosphate (IP3) production, and cytoplasmic Ca2+ concentration ([Ca2+]1) in cultured aortic smooth muscle cells were compared with those of other agonists. ET-1 induced contractions of the MRVs, which were slow in onset, but reached a similar maximum amplitude (at 10 nM ET-1) as that seen with norepinephrine (NE, 10 microM) or [arg8]vasopressin (AVP, 0.1 microM). The EC50 for ET-1 was 1.3 +/- 0.1 nM. Removal of extracellular Ca2+ reduced ET-1-induced contractions to 11 +/- 3% of those in Ca2+-containing medium. With NE, the same procedure reduced contractions to 47 +/- 7% of those in Ca2+-containing medium, while with AVP, the reduction was similar in magnitude to that induced by ET-1 (11 +/- 5% of those in Ca2+-containing medium). Relaxation of ET-1-induced and NE-induced contractions by diltiazem was not complete (maximal at 58 +/- 6% with 10 microM diltiazem after 6 nM ET-1, and at 70 +/- 3% after 0.1 microM NE), in contrast to that of 80 mM K+-induced contractions, which were potently (IC50 = 0.2 microM) and completely reversed (100% relaxation at 10 microM diltiazem). ET-1 (6 nM) caused a small but significant depolarization of the MRVs (approximately 7 mV), the magnitude of which was only about one-third of that induced by equieffective contractile concentrations of NE and AVP. The voltage-sensitive Ca2+ channel agonist Bay K 8644 (1 microM), in contrast to ET-1, NE, and AVP, produced a small contraction (30 +/- 2% of the maximum response to NE), but no further depolarization when added in the presence of 15 mM K+ (which elicited approximately 12 mV depolarization but no contraction).(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1989
PMID:The mechanism of action of endothelin-1 as compared with other agonists in vascular smooth muscle. 247 23

The effect of atrial natriuretic peptide (ANP) on cytosolic free calcium ([Ca2+]i) was studied in monolayers of cultured vascular smooth muscle (VSM) cells loaded with a fluorescent calcium indicator, fura-2. ANP (atriopeptin III, 10(-8) M) decreased the resting level of [Ca2+]i and sustained rises in [Ca2+]i following peak levels induced by vasoconstrictive hormones (angiotensin II or vasopressin). ANP also decreased a rise in [Ca2+]i induced by high potassium (high K+) depolarization. The initial rise in [Ca2+]i induced by vasopressin was not inhibited by ANP. On the other hand, calcium antagonists (nicardipine or nifedipine) inhibited the high K+-induced rise in [Ca2+]i, whereas there was no effect on rises in [Ca2+]i induced by vasopressin. These results suggest that calcium antagonists inhibit voltage-dependent calcium channels, while ANP can decrease [Ca2+]i presumably through a stimulation of calcium-extrusion active transports in vascular smooth muscle cells.
J Cardiovasc Pharmacol 1989
PMID:Difference between the effects of atrial natriuretic peptide and calcium antagonist on cytosolic free calcium in cultured vascular smooth muscle cells. 247 40

Patients with chronic heart failure (CHF) have increased plasma levels of the antidiuretic hormone arginine vasopressin (AVP). The stimulus for increased AVP secretion is unknown, but appears to involve a nonosmotic drive which alters normal osmoregulatory mechanisms. Centrally acting alpha 2-adrenergic agonists suppress AVP secretion in experimental animals. To examine the hypothesis that such effects might be apparent on the chronically elevated AVP levels in patients with CHF, we measured AVP, heart rate (HR), mean arterial pressure (MAP), and plasma norepinephrine (NE) after 4 mg oral guanabenz in nine patients with this disease. Plasma NE decreased from 513 +/- 131 to a minimum of 371 +/- 117 pg/ml (p less than 0.02) 5 h postdrug. HR decreased from 80 +/- 9.3 to 74 +/- 10 beats/min (p less than 0.05) and MAP decreased from 88 +/- 8.5 to 83 +/- 10 mm Hg (p less than 0.05). Plasma AVP, however, did not change from baseline levels of 5.6 +/- 1.6 pg/ml. Serum osmolality was also constant. These data do not support a possible role for acute increases of alpha 2-adrenergic activity in suppressing the increased plasma AVP levels of CHF, at least under basal conditions at constant osmolality.
J Cardiovasc Pharmacol 1989 Sep
PMID:Alpha 2-adrenergic stimulation and vasopressin in congestive heart failure. 247 22


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