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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The role of vasopressin in blood pressure control and in the pathogenesis of one-kidney Goldblatt hypertension in the conscious dog was investigated. 2. Infusion of synthetic arginine vasopressin to elevate plasma levels approximately five-fold caused bradycardia in normal dogs and increase in mean arterial blood pressure in dogs with pharmacological autonomic blockade. 3. A similar degree of elevation of plasma vasopressin concentration was observed after mild non-hypotensive haemorrhage. 4. Renal artery constriction in unilaterally-nephrectomized dogs caused a rise in plasma renin activity and only a doubling of plasma vasopressin concentration, but a marked rise in mean arterial blood pressure. 5. Vasopressin may play a role in normal cardiovascular homeostatic responses, but its role in the pathogenesis of this form of hypertension is unlikely to be significant.
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PMID:The role of vasopressin in blood pressure control and in experimental hypertension. 28 63

The concentration of blood vasopressin was investigated in apparently healthy persons and in patients with I--II degree hypertension, aged from 20 to 80 years. Vasopressin concentration was determined by the biological method according to the antidiuretic effect of ethanol-anesthetized and constantly hydrated rats on an original 5-channel apparatus. The results obtained showed the blood vasopressin concentration to increase with age. In patients with the I--II degree hypertensive disease the mentioned concentration was significantly higher than in healthy persons of the same age. Close correlation coefficient was revealed between the blood vasopressin concentration and minimal arterial blood pressure values.
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PMID:[Blood vasopressin concentration is patients of different ages with hypertension]. 47 71

Several recent reports have suggested that pressor hormones may be released during and after carotid endarterectomy and that release of these factors may be associated with postoperative hypertension and other postoperative morbidity. We measured vasopressin, adrenocorticotropic hormone, and cortisol in jugular venous blood during carotid endarterectomy under general anesthesia in 43 patients with routine carotid shunting. Jugular venous vasopressin increased significantly after the second period of carotid occlusion for shunt removal and remained increased at closure. Vasopressin did not change during the initial carotid occlusion for shunt placement or during the endarterectomy itself, and neither ACTH nor cortisol changed at any sample time. Greater resting vasopressin and cortisol and larger responses of vasopressin were observed in patients receiving phenylephrine to correct intraoperative hypotension. There were no correlations between postoperative hypertension or postoperative complications and intraoperative hormone values. These results suggest (1) basal intraoperative vasopressin values reflect the blood volume of the patient, (2) increased vasopressin was not related to postoperative morbidity, and (3) intraoperative increases in pressor hormones are most likely physiologic responses to specific stimuli such as hypovolemia or hypotension rather than pathologic phenomena. We speculate that the increase of vasopressin after the second carotid occlusion and reperfusion of the brain may be due to the action of humoral factors released into the carotid circulation from the endarterectomy site.
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PMID:Jugular venous vasopressin increases during carotid endarterectomy after cerebral reperfusion. 161 7

In previous studies we found that vasopressin stimulation of both cyclic AMP (cAMP) formation in cortical collecting tubules (CCT) and sodium reabsorption in isolated perfused kidneys was markedly exaggerated in rats with mineralocorticoid hypertension. In the present study, we tested the response (cAMP accumulation) of cortical and outer medullary collecting tubules (OMCT) to vasopressin in two rat models that are resistant to deoxycorticosterone acetate (DOCA)-induced hypertension, the Wistar-Furth strain and NaCl-deficient rats. The blood pressure of normal outbred Wistar rats rose to hypertensive levels (systolic pressure more than 165 mm Hg) during a 5-week treatment with DOCA (10 mg/week) and 1% saline to drink. Significant hypertrophy of the heart and kidneys was also observed. Vasopressin (10(-8) M)-induced cAMP formation was enhanced 3.4-fold in the CCT (OMCT unchanged) of hypertensive rats compared with normotensive controls. Significant hypertrophy (as indexed by tubule diameter) of the CCT but not the OMCT was also observed in DOCA-salt hypertensive rats. Restriction of dietary NaCl (0.13% in chow, tap water to drink) completely prevented DOCA-induced hypertension, organ and CCT hypertrophy, and enhancement of vasopressin-stimulated cAMP formation in the CCT. In Wistar-Furth rats, DOCA-salt treatment did not alter blood pressure or cause significant organ hypertrophy. However, DOCA-salt treatment enhanced vasopressin-stimulated cAMP formation by 4.1-fold in CCT of Wistar-Furth rats, with significant tubular hypertrophy in the CCT but not the OMCT. We conclude that DOCA-induced hypertension and changes in CCT function are dependent on excess dietary NaCl.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1991 Jan
PMID:Vasopressin response in collecting ducts of rats resistant to mineralocorticoid hypertension. 184 20

Vasopressin acts at a number of sites in the central nervous system to alter arterial pressure. This study investigated the hypothesis that vasopressin acts at the rostral ventrolateral medulla to increase arterial pressure. The rostral pressor area of the medulla oblongata was exposed in urethane-anesthetized rats prepared for topical application of vasopressin. A 3-minute application of vasopressin (range 10(-8) to 10(-3) M) produced dose-dependent increases in arterial pressure that averaged between 2 +/- 1 and 65 +/- 11 mm Hg (p less than 0.01). Tachycardia was not a consistent response at any concentration of vasopressin. Intravenous administration of a V1 vasopressin antagonist did not modify the pressor response produced by topical application of vasopressin (10(-4) M). Application of the V1 antagonist to the rostral pressor area, however, prevented the production of a pressor effect to subsequent topical application of vasopressin (10(-4) M). These experiments suggest that vasopressin stimulates the activity of vasomotor neurons in the rostral ventrolateral medulla by a mechanism that involves a neuronal V1 receptor.
Hypertension 1990 Feb
PMID:Cardiovascular actions of vasopressin at the ventrolateral medulla. 196 90

Renomedullary interstitial cells cultured from the Dahl salt-resistant rat have higher levels of basal cytosolic calcium and prostaglandin E2 and are more responsive to vasopressin than interstitial cells from the Dahl salt-sensitive rat. We examined the potential role of inositol phospholipid hydrolysis in mediating these differences. Vasopressin-induced increases in labeled inositol phosphates were enhanced in renomedullary interstitial cells from Dahl salt-resistant compared with those from salt-sensitive rats. Addition of neomycin reduced basal production of labeled inositol phosphates and abolished the increase in inositol phosphates induced by vasopressin. Neomycin also prevented the peak decline pattern in cytosolic Ca2+ seen with vasopressin but did not influence basal cytosolic Ca2+. In the presence of neomycin, vasopressin induced a modest but prolonged increase in cytosolic calcium. In contrast to its marked effects on inositol phosphate production, neomycin was without effect on basal or vasopressin-responsive prostaglandin E2 production. Moreover, basal and vasopressin-induced increases in cytosolic Ca2+ remained higher in renomedullary interstitial cells from Dahl salt-resistant versus those from salt-sensitive rats exposed to neomycin. The results do not support a requirement for phospholipase C-induced inositol phospholipid hydrolysis in the mediation of vasopressin actions on prostaglandin E2 production by renomedullary interstitial cells and imply that the differences in cytosolic Ca2+ and prostaglandin E2 seen in these two cell lines are not related to differences in inositol phospholipid metabolism.
Hypertension 1991 Mar
PMID:Calcium and prostaglandin E2 in renomedullary interstitial cells. 199 61

Reduced homeostatic capacity is typical of the aging process and is particularly apparent in changes in the neuroendocrine control of cardiovascular homeostasis. Not only is there reduced beta-adrenoceptor responsiveness, but reduced baroreflex function also occurs with age. These result in increased sensitivity to the therapeutic and postural hypotensive effects of diuretics and vasodilators. Increased total body sodium and reduced activity of the renin-angiotensin-aldosterone system may also contribute to the therapeutic effect of diuretics and salt restriction in elderly hypertensives. In addition, atrial natriuretic peptide levels are increased in the elderly and may in part be responsible for the suppressed renin and aldosterone levels found in older groups. Vasopressin secretion and thirst are also disturbed with age, and may act in concert with declining renal function to predispose the elderly to disturbances of water balance. An understanding of these neuroendocrine changes with age is important to maximize therapeutic benefit and to minimize adverse effects in the treatment of hypertension in the elderly.
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PMID:Neuroendocrine mechanisms and cardiovascular homeostasis in the elderly. 200 44

Recent studies suggest that humoral and endothelium-dependent mechanisms may play an important role in the cerebral circulation. Angiotensin may acutely and chronically increase resistance of large cerebral arteries and reduce cerebral microvascular pressure without changing cerebral blood flow. We hypothesize that the brain may sense reductions in microvascular pressure and initiate compensatory neurohumoral responses to raise arterial pressure. Vasopressin appears to play an important role in regulation of production of cerebrospinal fluid and brain fluid volume. Vasopressin also may be protective when intracranial pressure is elevated. Endothelium-dependent mechanisms also may have important influences on tone of cerebral vessels. Synthesis of the endothelium-derived relaxing factor nitric oxide, or a nitric oxide-containing compound, appears to influence both basal tone and responses of large cerebral arteries to acetylcholine in vivo. Large cerebral arteries dilate in response to increased blood flow in vivo, and this response may be mediated in part by release of a humoral factor by endothelium. Endothelium-dependent responses of cerebral arterioles to receptor- and nonreceptor-mediated agonists are impaired during chronic hypertension. The mechanism of impairment of endothelium-dependent responses of cerebral arterioles appears to involve production of an endothelium-derived contracting factor.
Hypertension 1991 Jun
PMID:Regulation of cerebral blood vessels by humoral and endothelium-dependent mechanisms. Update on humoral regulation of vascular tone. 204 73

The purpose of this study was to examine pressor hormones and platelet alpha 2-adrenergic receptors in elderly unmedicated free-living subjects. Eighty-seven subjects, 70 +/- 5 years old (mean +/- SD), hypertensive or normotensive (blood pressure less than 160/90 mm Hg) were recruited for measurement of blood levels of norepinephrine, epinephrine, and vasopressin, as well as density and affinity of alpha 2-adrenergic receptors from platelet membranes, assessed by maximal binding (Bmax) and dissociation constant (Kd) of rauwolscine. They were separated into white hypertensive (n = 22) or normotensive (n = 41), and black hypertensive (n = 11) or normotensive (n = 13) groups, with similar age distribution throughout and similar blood pressure levels in the hypertensive and normotensive groups. Vasopressin was higher in the black hypertensive than white hypertensive group (1.5 +/- 1.0 vs. 0.7 +/- 0.5 pg/ml, respectively, p less than 0.005), whereas epinephrine correlated inversely with diastolic blood pressure (r = -0.7, p less than 0.02, in the black hypertensive group). Kd was higher in the black normotensive group than in the other groups (1.6 +/- 0.6 vs. 1.0 +/- 0.2, 1.1 +/- 0.3, or 1.0 +/- 0.3 nM in the white normotensive, black hypertensive, or white hypertensive group, respectively, p less than 0.002). Bmax was no different among groups but was significantly correlated with vasopressin levels for the whole group (r = 0.4, p less than 0.0004) although no such correlation existed within the black hypertensive group. The data suggest that various vasoconstrictor systems participate to different extents in the mechanisms generating and sustaining hypertension in elderly white and black subjects.
Hypertension 1990 Feb
PMID:Pressor hormones in elderly hypertensive persons. Racial differences. 215 31

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.
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PMID:Osmoregulation and baroregulation of plasma vasopressin in essential hypertension. 243 80


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