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

To gain insight into the mechanisms that could account for the augmentation of cellular reactivity in primary hypertension, we have examined some of the biochemical events which are implicated in the transmission of mitogenic signal as well as in cell reactivity. This study focussed on phospholipase C, protein kinase C and GTP-binding proteins (G-proteins), in response to thrombin or arginin-vasopressin (AVP). Cultured fibroblasts prepared from the adventitia of thoracic aorta of spontaneously hypertensive rat (SHR) were used as cell models and were compared with fibroblasts prepared from controls Wistar-Kyoto (WKY) rats. The mitogenicity of each agonist was estimated by measuring the incorporation of 3H-thymidine into the newly synthesized DNA. The agonist-induced phospholipase C activity was evaluated by measuring the production of 3H-inositol phosphates in cells prelabeled with 3H-inositol. The influence of protein kinase C and that of G proteins on the mitogenesis in cells stimulated by thrombin or AVP was determined by pretreating cells with phorbol 12-myristate, 13-acetate (TPA) and pertussis toxin, respectively. Kinetics and dose response studies have demonstrated that in response to thrombin and AVP, the phospholipase C activity and the incorporation of 3H-thymidine were significantly higher in the fibroblasts derived from SHR.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Activation mechanisms by thrombin and vasopressin of fibroblasts in spontaneously hypertensive rats]. 195 75

In the past several years, investigators have given evidence that vasopressin (VP), in addition to its antidiuretic function, may play an important role in cardiovascular regulation through other mechanisms. An increased plasma VP level has been reported in some patients with mild-to-moderate essential hypertension (EH). Additionally, yohimbine, a selective alpha 2-adrenoceptor antagonist, has been shown to increase the plasma VP level and blood pressure (BP) in man. The present study was performed to evaluate the effects of chronically administered guanfacine, a centrally acting alpha 2-adrenoceptor agonist, on high plasma VP levels in patients with mild-to-moderate EH in whom no other causes responsible for elevated plasma VP levels were present. The relations among VP, BP and renin-angiotensin-aldosterone system were also investigated. Eleven patients (8 women and 3 men aged 62 +/- 3 years) with untreated and uncomplicated EH were included in the study after a 2-week placebo period and kept on a diet containing 120 mmol sodium and 80 mmol potassium daily. In all patients treated once daily with 1 mg of guanfacine for 4 weeks, the drug-induced changes in plasma levels of VP and aldosterone (ALD), plasma renin activity (PRA), plasma osmolality, BP and heart rate were determined. A marked reduction in plasma VP levels (p less than 0.001) was observed and this was accompanied by a significant fall in mean arterial blood pressure (p less than 0.001). No significant changes in heart rate, plasma osmolality, PRA and plasma ALD levels were found. The results suggest that guanfacine might suppress VP secretion via alpha 2-adrenoceptors without significantly affecting renin-angiotensin-aldosterone system.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The effect of chronic guanfacine administration on high plasma vasopressin levels in essential hypertension. 240 71

The renin-angiotensin system has a range of physiological actions concerned with the control of the circulation. Angiotensin II has both an immediate and a delayed pressor effect; it stimulates the secretion of aldosterone and antidiuretic hormone, promotes thirst, stimulates the sympathetic nervous system at various sites while inhibiting vagal tone, and has a range of direct effects on the kidney. Several aspects of this range of actions can become deranged in a number of forms of hypertension as well as in congestive cardiac failure. Hence much effort has been directed in recent years to the development of agents designed to interfere with the renin-angiotensin system and to apply these clinically in the treatment of hypertension and congestive cardiac failure. Orally active converting enzyme inhibitors are of proven benefit not only in renovascular hypertension, but also, when combined with loop diuretics, in the treatment of intractable hypertension as well as, both alone and in combination with thiazide diuretics, in the treatment of essential hypertension. In congestive cardiac failure controlled trials have shown that converting enzyme inhibitors can improve exercise tolerance while diminishing lassitude, correct potassium deficiency, and limit ventricular arrhythmias. Energetic efforts are being made to develop orally active inhibitors of the enzyme renin itself, since these should be more specific in action than the presently available and very successful converting enzyme inhibitors.
 ...
PMID:Circulatory basis for the use of angiotensin converting enzyme inhibitors in hypertension and cardiac failure. 242 88

The adenylate-cyclase activator forskolin, the guanylate-cyclase stimulator sodium nitroprusside, the phosphodiesterase inhibitor Ro 15-2041, different Ca-entry blockers, as well as various vasodilators, and the atrial natriuretic peptide were tested for antiplatelet activity. Thrombin, vasopressin, ADP, arachidonic acid, and the dihydropyridine Ca agonist CGP 28392 were used as platelet activators. The physiological and biochemical parameters of platelet function studied included shape-change reaction, intracellular free-Ca modulation, and cyclic nucleotide formation. When inhibition of the shape-change response occurred, it was accompanied by inhibition of the increase in intracellular free Ca. Furthermore, the results suggest a possible intracellular site of action of Ca entry blockers in platelets, and confirm the importance of modulation of cyclic nucleotides in the regulation of platelet function, regardless of the mechanism of platelet activation. Additional antiplatelet activity of antihypertensive agents may have a beneficial effect in reducing the associated risk of thrombo-embolic complications in essential hypertension.
 ...
PMID:Vasodilating agents and platelet function: intracellular free calcium concentration, cyclic nucleotides, and shape-change response. 243 9

The role of vasopressin in human hypertension was examined in a series of studies. In patients with primary hyperaldosteronism and benign essential hypertension, circulating vasopressin was generally lower than in normotensive subjects. In contrast, plasma vasopressin was increased (p less than 0.001) in patients with malignant-phase hypertension. However, compared to infused vasopressin in normal subjects, when plasma levels of up to 120 pg/ml did not affect blood pressure, the increased levels found in malignant hypertension could not account for the hypertension. The possibility that there may be an increased pressor sensitivity to vasopressin in hypertension was examined by infusing the peptide into nine patients with essential hypertension. This showed a slight increase in sensitivity compared to normotensive subjects, but again this was insufficient to account for the discrepancy between the circulating level of vasopressin and the extent of the raised blood pressure in the hypertensive patients. The effect of chronically elevated levels of vasopressin was studied in a group of patients with the syndrome of inappropriate ADH excess as a consequence of bronchogenic carcinoma. In spite of having chronically elevated levels of vasopressin, these patients had normal blood pressures for their age and sex. Our results suggest that, although vasopressin is elevated in malignant hypertension, it does not contribute significantly to the raised blood pressure, and its increase is probably a consequence of volume shrinkage through renal salt and water loss.
 ...
PMID:Vasopressin and hypertension in man. 243 62

Vasopressin secretion is stimulated by hyperosmolality, hypovolemia, or hypotension and is inhibited by hypoosmolality, hypervolemia, or hypertension. These osmotic and hemodynamic influences are mediated by neuronal afferents that originate in separate osmoreceptors or baroreceptors but ultimately converge to act on the same neurosecretory neurons. Functionally, the two control systems are integrated in such a way that osmoregulation is altered but not disrupted by hemodynamic influences. In patients with uncomplicated essential hypertension, basal as well as osmotically stimulated vasopressin is completely normal. The vasopressin response to an acute reduction in blood pressure is also normal if the values are expressed relative to the change in pressure. However, if the plasma vasopressin response is plotted as a function of absolute blood pressure, the line describing the relationship lies well to the right of normal. Thus, although it is completely intact, the baroregulatory mechanism appears to be reset to a higher level in essential hypertension. These results suggest that increased secretion of vasopressin does not contribute to the genesis or maintenance of uncomplicated, untreated essential hypertension but may antagonize the therapeutic effect of some antihypertensive drugs. If so, antagonists of V1 receptors may be useful as second-line adjunctive therapy for this condition.
 ...
PMID:Osmoregulation and baroregulation of plasma vasopressin in essential hypertension. 243 80

A study was made of the effect of a single intake of captopril on the neurohumoral mechanisms of the regulation of renal circulation in 25 patients with essential hypertension (EH). Captopril induced an increase of the effective renal blood flow (ERB) and of the effective renal plasma flow along with a considerable lowering of the renal vascular resistance. No relationship was found between these changes and the time course of changes in the activity of plasma renin, aldosterone and vasopressin concentration in blood plasma. The relationship was established between the changes in the ERB and the time course of changes in baroreceptor sensitivity that significantly increased in the majority of EH patients under the effect of captopril.
 ...
PMID:[Neurohumoral mechanisms regulating renal blood circulation in patients with hypertension undergoing captopril block of angiotensin-converting enzyme]. 257 61

As many as 52 patients with essential hypertension aggravated by circulatory failure were examined for the clinical, hemodynamic and neurohumoral parameters during furosemide stimulation. In elderly patients, the optimal vasodilatory dose of nifedipine amounted to 10 mg, that of verapamil to 40 mg per os or to 5 mg i.v. In patients with the stimulated activity of plasma renin, the concentration of plasma aldosterone remained unchanged. The plasma concentrations of ACTH and cortisol tended towards increase while vasopressin concentration dropped. Side effects could be frequently observed. Hemodynamic shifts appeared to be negative. During the first hour, forced diuresis was recorded. In patients with unstimulated plasma renin activity, plasma aldosterone concentration declined, whereas the concentrations of ACTH, cortisol and vasopressin rose. Side effects were less in number, the hemodynamic shifts were positive, and diuresis turned out 2-3 times less during the first hour than within the next 4 hours. It is suggested that the efficacy of the treatment with calcium antagonists can be predicted according to the magnitude of the hourly diuresis with regard to the type of hemodynamics.
 ...
PMID:[The efficacy of calcium antagonists in circulatory failure in elderly patients with hypertension]. 262 43

Effects of a single administration of captopril on plasma and urinary vasopressin (AVP) were examined in 8 normotensive (NT) female volunteers, 17 patients with essential hypertension (EHT) and 2 patients with primary aldosteronism (PA). Orally-administered captopril (25 mg) had no effect on plasma AVP levels in the three groups. However, urinary excretion of AVP decreased significantly after use of captopril in both NT and EHT subjects (-57% and -67%, respectively), and also in PA subjects. The magnitude of reduction in urinary AVP was significantly correlated with the pretreatment levels of plasma renin activity (r = 0.85) and plasma aldosterone concentration (r = 0.88) in NT subjects. Such correlation was not found in EHT subjects. These results suggest that captopril decreases AVP secretion in both normotensive and hypertensive subjects, but the relation of the magnitude in AVP reduction by captopril to the peripheral renin-angiotensin system might be different.
 ...
PMID:Effect of single-administration captopril on plasma and urinary vasopressin in normotensive subjects and patients with essential hypertension and primary aldosteronism. 269 64

Platelet activation factor (PAF)-, ADP and vasopressin-induced increments of platelet Ca2+ concentration were measured by quin-2 in 64 patients with essential hypertension and 16 normal donors. Basal concentration of free Ca2+ was 87 +/- 4 nM in donors, 106 +/- 5 nM in patients with labile hypertension (LH) and 122 +/- 6 nM in those with stable hypertension (SH) (p less than 0.01). PAF, ADP and vasopressin, added to platelets, increased [Ca]in by 448 +/- 58, 397 +/- 66, and 277 +/- 50 nM, respectively, in the donors, by 473 +/- 57, 479 +/- 54 and 195 +/- 32 nM, in LH patients, and by 607 +/- 85, 584 +/- 73 and 245 +/- 41 nM in SH patients. There were no significant variations between the three samples, using the ANOVA test. In 20 patients, whose both parents had essential hypertension, [Ca]in increment was 738 +/- 8 nM for PAF, 682 +/- 90 nM for ADP, and 320 +/- 61 nM for vasopressin. In 19 patients, who admitted to no essential hypertension in the family, these parameters were significantly lower: 310 +/- 40 nM for PAF, 389 +/- 61 nM for ADP, and 147 +/- 26 nM for vasopressin. The demonstrated changes may be making an important contribution to the maintenance of elevated vascular tone and provide an evidence in favor of a genetically-predetermined EH variety.
 ...
PMID:[Receptor-dependent regulation of the concentration of Ca2+ in the cytoplasm of thrombocytes in hypertensive patients]. 284 37


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>