Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A number of experiments were performed in order to investigate the possible importance of vasopressin (AVP) in the pathogenesis of high blood pressure in spontaneously hypertensive rats of the stroke prone strain (SHRSP). Radioimmunological studies revealed reduced concentrations of AVP in the plasma and brain of SHRSP as compared to normotensive controls. Intravenous administration of an AVP pressor antagonist had no significant influence on mean arterial blood pressure, cardiac output and total peripheral resistance in SHRSP. Crossbreeding of SHRSP with rats homozygous for hypothalamic diabetes insipidus resulted in the development of a new strain of rats which show high blood pressure despite of a complete lack in AVP. These results argue strongly against a pressor role of AVP in the development or maintenance of hypertension in SHRSP.
 ...
PMID:Pathogenesis of hypertension in spontaneously hypertensive rats: definite evidence against a pressor role of vasopressin. 669 49

A 2-hr 0.85 M hypertonic saline infusion was administered to ten normotensive volunteers and ten mildly hypertensive subjects to compare in these two groups the osmoregulation of vasopressin and the effect of this hormone on BP. No significant alteration in BP was observed in either group, despite markedly enhanced vasopressin levels. Significant positive correlations between plasma vasopressin (AVP) and plasma osmolality (POsm) were demonstrated in the controls (AVP = -70 + 0.25 POsm, r = 0.68, P less than 0.0001) and in the hypertensive group (AVP = -46 + 0.16 POsm, r = 0.59, P less than 0.0001). However, the vasopressin response to the osmotic stimulus was buffered in the hypertensive subjects; the slope of the regression line between plasma vasopressin and plasma osmolality was less steep in hypertensive subjects than in normotensive subjects (0.16 vs. 0.25, P less than 0.018). During the saline infusion the renal parameters were identical in the two groups. Finally, in mild hypertension, the osmoregulation of vasopressin was preserved but buffered and renal sensitivity to this hormone was normal. An osmotically induced physiological increase in vasopressin did not raise BP in either normotensive or mildly hypertensive subjects.
 ...
PMID:Osmoregulation and renal effects of vasopressin in normal and mildly hypertensive subjects. 672 36

Of 103 borderline essential hypertensives below the age of 36 years, 11 (10.7%) showed low renin, 57 (55.4%) showed normal renin, and 35 (33.9%) showed high renin. Various hormones such as plasma catecholamines, PA, DOC, B, cortisol 18-OH-DOC, 18-OH-B, ACTH, AVP and PRL tended to be high in the high renin group and tended to be low in the low renin group. Furthermore, urinary excretion of kallikrein was also increased in the high renin group and reduced in the low renin group. There was no hormone which was increased in the low renin group. Regardless of renin levels, pressor responses to exogenous angiotensin II were increased in these juvenile essential hypertensives. From these studies on endocrine factors it is concluded that essential hypertensives are largely divided into 3 groups; the high hormone group, the normal hormone group and the low hormone group, and increased hormones may play an important role in the development of hypertension in the high hormone group. However, in the low hormone group and a part of the normal hormone group the mechanism of hypertension cannot be revealed by the study on endocrine factors.
 ...
PMID:Endocrine factors in juvenile essential hypertension. 675 Jan 91

We have studied plasma and cerebrospinal fluid vasopressin (CSF-AVP) and osmolality in 28 patients with cervical or lumbar pain syndromes (control patients), 11 patients with normal pressure hydrocephalus (NPH) and in 5 patients with benign intracranial hypertension (BIH). Vasopressin concentration in lumbar CSF to a high extent reflected the actual ventricular CSF-AVP concentration. In all groups CSF-AVP was lower than plasma AVP. Mean CSF-AVP in the control group was 1.3 pg/ml +/- 0.1 (SEM). In the NPH patients, who all suffered from severe dementia, CSF-AVP level was not different from that found in the control group (1.4 pg/ml +/- 0.2). In contrast to the findings in the two other groups CSF osmolality in BIH patients was higher than plasma osmolality (P less than 0.0). CSF-AVP in the BIH patients, characterized by an elevated intracranial pressure (ICP), was higher than in the control group (2.7 pg/ml +/- 0.4, P less than 0.001).
 ...
PMID:Vasopressin in the cerebrospinal fluid of patients with normal pressure hydrocephalus and benign intracranial hypertension. 711 92

A humoral factor has been implicated in Dahl salt-sensitive genetically hypertensive rats. The goal of this study was to evaluate the pressor role of vasopressin (AVP) in Dahl rats. Salt-sensitive (S) and resistant (R) rats were fed either high (8%) or low (.04%) NaCl diets for 6 to 8 weeks. Blood pressure was elevated in S rats fed high salt diets (p less than 0.05). Plasma AVP increased with high salt diet in both groups (p less than 0.05), but was higher in S than R rats (2.0 +/- 0.3 and 1.3 +/- 0.2 microU/ml respectively, mean +/- SE, p less than 0.05). With low salt diet, plasma AVP did not differ significantly in S and R rats (1.0 +/- 0.2 and 0.7 +/- 0.2 microU/ml respectively). Pressor responses to intravenous injection of AVP were greater in S than R rats (p less than 0.05), but this difference was also observed with pressor responses to norepinephrine (S greater than R, p less than 0.05); there was no difference in pressor responses to AVP in S rats fed high vs low salt diet. Injection of 50 micrograms of d(CH2)5 VDAVP, which selectively inhibits vasoconstrictor effects of AVP, failed to lower blood pressure in S and R rats fed high or low salt diets despite the fact that this dose decreased pressor responses to 8 microU of AVP more than 90%. Although plasma AVP and vasopressor responses to AVP and NE are slightly elevated in S rats fed high salt, results with d(CH2)5 VDAVP suggest that vasoconstrictor effects of AVP do not play an important role in the maintenance of hypertension in Dahl S rats.
Hypertension
PMID:Does vasopressin contribute to salt-induced hypertension in the Dahl strain? 721 72

10 patients with renovascular hypertension (HRV) and 12 healthy persons were examined under water immersion (WI) conditions without and after blockade of opioid receptors with 2 mg of naloxone. Blood pressure, body mass, change of plasma volume, plasma molality, PRA, and serum values of AVP, aldosterone and catecholamines were evaluated. There were no significant changes between the two examined groups before and after WI. It seems that the drop in blood pressure induced by WI is not only the result of diminished activation of RAAS. The role of opioid receptors in controlling blood pressure and other evaluated parameters is likely in both examined groups.
 ...
PMID:[The influence of opioid receptor blockade on the behavior of selected biochemical and hormonal parameters in patients with renovascular hypertension studied under water immersion conditions]. 756 83

We investigated the genesis of the hypertensive response to acute (45 min) aortic constriction in two models of chronic vasopressin (AVP) deficiency, i.e., Brattleboro strain and median eminence lesioned (MEL) Wistar rats. The same degree of partial aortic constriction, with a pneumatic cuff placed around the abdominal aorta, yielded a sudden and maintained increase in carotid pressure to the same extent in Brattleboro, MEL and sham-MEL rats. Blockage of AVP V1 receptors with d(CH2)5Tyr[Me]AVP did not affect the hypertensive response of Brattleboro or MEL rats, but gradually blunted the response of sham-MEL rats. Blockage of angiotensin II receptors with saralasin blunted the hypertensive response of the AVP-deficient subjects throughout the experiment, but only delayed (5-15 min) the onset of hypertension in sham-MEL rats. Simultaneous blockage of AVP and angiotensin II blunted the hypertensive response of sham-MEL and AVP-deficient rats throughout the experiment. These data demonstrate that when one vasoactive system is chronically absent, as is the case for AVP in Brattleboro and MEL rats, the renin-angiotensin system plays the major role in the pathophysiology of acute aortic coarctation hypertension.
 ...
PMID:Hypertensive response to acute aortic coarctation in chronic vasopressin deficient states. 758 Dec 64

To examine the role of vasopressin (AVP) receptors in the regulation of the hemodynamics and release of atrial natriuretic peptide (ANP), and the participation of renal nerve inputs in the osmotic AVP release, hypertonic saline (HS) was infused into conscious, bilaterally nephrectomized rats with non-peptide, selective antagonists for the V1-receptor or V2-receptor of AVP. In the control group, HS alone increased mean arterial pressure, plasma ANP and AVP, plasma volume and plasma osmolality, and decreased the heart rate. In the V1-receptor antagonist group, an increase in the mean arterial pressure and a decrease in heart rate were completely abolished and an increase in plasma ANP was attenuated. In the V2-receptor antagonist group, increases in mean arterial pressure and plasma ANP and a decrease in heart rate were attenuated. However, the ratio of the changes in heart rate to the changes in mean arterial pressure in the V2-receptor antagonist group is significantly higher than that in the control group. In both experimental groups, increases in plasma AVP, plasma volume and plasma osmolality were not different from those in the control group. These results suggest that a HS-induced increase in mean arterial pressure is mediated by the pressor effect of AVP, mainly through V1-receptors, and that the depressor effect of AVP through V2-receptors may not influence tonically HS-induced hypertension. Moreover, HS-induced increase in plasma ANP is mediated mainly by increases in plasma volume and blood pressure, but may not be affected by a direct action of AVP to the heart. Renal afferent nerve inputs may not have effects on the regulation of osmotic AVP release.
 ...
PMID:Effects of V1- and V2-vasopressin (AVP) antagonists on the pressor, AVP and atrial natriuretic peptide responses to a hypertonic saline infusion in conscious anephric rats. 762 34

The present study was designed to investigate the effect of a lack of vasopressin resulting from electrolytic lesion of the median eminence of the hypothalamus on the acute 45-min aortic coarctation hypertension elicited in conscious rats by means of a pneumatic cuff placed around the aorta above the renal arteries. Forty-eight hours after lesion, aortic constriction elicited a prompt (5-min) rise in mean carotid pressure from 115 +/- 2 to 149 +/- 2 mmHg, followed by a gradual decline to 129 +/- 2 mmHg. In contrast, sham-lesioned rats exhibited a prompt hypertensive response from 118 +/- 2 to 157 +/- 2 mmHg that leveled off throughout the experiment. Lesioned rats treated with saralasin presented a blunted hypertensive response (within 125 +/- 2 to 130 +/- 2 mmHg), whereas sham-lesioned rats showed only a delay in the onset of hypertension. The hypertensive response of lesioned rats was unaffected by the vasopressin antagonist [d(CH2)5Tyr(Me)]AVP, whereas sham-lesioned rats submitted to this treatment presented a prompt rise in pressure followed by a gradual decline at the end of the experiment. Lesioned and sham-lesioned rats treated with saralasin plus vasopressin antagonist showed a blunted hypertensive response throughout the experiment. These data demonstrate that the integrity of the median eminence plays a pivotal role in the maintenance (30-45 min) of acute aortic coarctation hypertension, presumably involving the release of vasopressin from the neurohypophysis, whereas angiotensin II mainly accounts for the prompt (5-15 min) rise in pressure.
 ...
PMID:Effect of median eminence lesion on the hypertensive response due to acute aortic coarctation. 809 20

Exogenous vasopressin decreases blood flow to the choroid plexus and production of cerebrospinal fluid. Some studies indicate that hypoxia and increases in intracranial pressure (ICP) produce increases in circulating vasopressin. We examined the hypothesis that endogenous release of vasopressin decreases blood flow to the choroid plexus during hypoxia and increased ICP. Blood flow to the choroid plexus was measured in anesthetized rabbits using microspheres. Hypoxia increased cerebral blood flow more than twofold but had little effect on blood flow to the choroid plexus. In contrast, hypoxia produced a marked increase in blood flow to the choroid plexus in the presence of a vasopressin V1-antagonist, [d(CH2)5Tyr(Me)]AVP. During intracranial hypertension, blood flow to the choroid plexus decreased from 409 +/- 42 to 295 +/- 25 ml.min-1 x 100 g-1 (means +/- SE; P < 0.05 vs. control) when ICP was increased from 1 to 40 mmHg. The vasopressin antagonist inhibited the decrease in blood flow to the choroid plexus in response to increased ICP. Thus release of vasopressin during hypoxia and increased ICP have a constrictor effect on blood vessels of the choroid plexus. Plasma levels of vasopressin increased minimally during hypoxia and increased ICP, which suggests that sources of vasopressin other than plasma affect blood vessels of the choroid plexus. We propose that endogenous vasopressin may play a protective role during hypoxia and intracranial hypertension by a negative feedback mechanism to reduce blood flow to the choroid plexus.
 ...
PMID:Effect of endogenous vasopressin on blood flow to choroid plexus during hypoxia and intracranial hypertension. 814 39


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