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

Vasopressin has been shown to elicit vasoconstriction in unanaesthetized animals at plasma concentrations similar to those associated with its renal antidiuretic effect. The vasconstrictor effects of vasopressin do not normally translate into pressor responses until relatively high plasma concentrations are reached. This appears to be related to very effective buffering by the baroreceptor reflex. In the absence of afferent signals from the baroreceptors (surgical denervation, but more importantly, low arterial pressure), the vasoconstriction elicited by vasopressin represents a significant part of the mechanisms that determine blood pressure. Vasopressin is clearly involved in the short-term control of blood pressure in situations such as haemorrhage, other volume-depleted states and dehydration. However, it is only one of several short-acting mechanisms which complement each other in the defence against hypotensive stresses. Under different conditions, the cardiovascular effects of vasopressin seem to have a component related to the central nervous system control of the circulation. Whether or not circulating vasopressin interacts with the newly described network of extrahypothalamic projections from the paraventricular nucleus is yet conjectural. However, the presence in the brain of vasopressin-containing pathways and of various types of receptors to vasopressin, as well as the existence of cardiovascular effects elicited by central administration of antidiuretic hormone, suggests a role for cerebral vasopressin in the control of autonomic function. Slightly elevated levels of vasopressin have been found in various forms of hypertension. Yet, the role of vasopressin, when present, may be more related to its antidiuretic than to its vasoconstrictor properties.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vasopressin in cardiovascular control: role of circulating vasopressin. 623 29

The role of vasopressin as a pressor agent to the hypertensive process was examined. Vasopressin plays a major role in the pathogenesis of DOCA-salt hypertension, since the elevation of blood pressure was not substantial in the rats with lithium-treated diabetes insipidus after DOCA-salt treatment. Administration of DDAVP which has antidiuretic action but minimal vasopressor effect failed to increase blood pressure to the levels observed after administration of AVP. Furthermore, the pressor action of vasopressin appears to be important in the development of this model of hypertension, since the enhanced pressor responsiveness to the hormone was observed in the initial stage of hypertension. Increased secretion of vasopressin from neurohypophysis also promotes the function of the hormone as a pathogenetic factor in hypertension. An unproportional release of vasopressin compared to plasma osmolality may be induced by the absence of an adjusting control of angiotensin II forming and receptor binding capacity for sodium balance in the brain. However, the role of vasopressin remains to be determined in human essential hypertension.
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PMID:Vasopressin as a possible contributor to hypertension. 632 16

To study the hypotensive mechanism of the new oral converting-enzyme inhibitor, MK-421, we evaluated the antihypertensive effect of MK-421 in rats with hypertension induced by chronic administration of norepinephrine (NE) or vasopressin and measured urinary kallikrein and kinin excretions as indices of the renal kallikrein-kinin system. When 6 mg/kg/day of MK-421 was administered simultaneously with 1.8 mg/kg/day of NE, the systolic blood pressure of conscious rats rose on Day 1 to only 122.6 +/- 3.4 mm Hg compared with the rise to 146.3 +/- 1.6 mm Hg when NE alone was infused (p less than 0.001). Similarly, when the same dose of MK-421 was administered simultaneously with 7.2 U/kg/day of vasopressin, the systolic blood pressure of conscious rats rose on Day 1 to only 117.4 +/- 3.8 mm Hg compared with the rise to 141.6 +/- 3.4 mm Hg when vasopressin alone was infused (p less than 0.01). The antihypertensive effect of MK-421 was sustained for 6 days in rats infused with NE or vasopressin. Infusion of NE alone resulted in a small but significant increase in urinary kallikrein excretion and no change in urinary kinin excretion. The combined administration of NE with MK-421 induced additional increases in urinary kallikrein and kinin excretions. Vasopressin alone resulted in marked decreases in urinary kallikrein and kinin excretions. The combined administration of vasopressin with MK-421 induced no additional changes in urinary kallikrein and kinin excretion. These results indicate that the hypotensive effect of MK-421 may depend on a reduced sensitivity of the peripheral arteries to vasoconstrictor substances.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:Antihypertensive effect of MK-421 in rats. Role of the renal kallikrein-kinin system. 632 17

1. Vasopressin deficient homozygous Brattleboro rats develop malignant renal hypertension following complete aortic-ligature between the renal arteries. 2. This form of hypertension is associated with high plasma renin activity (PRA) and plasma angiotensin II (AII) levels and a high incidence of the specific vascular lesions of fibrinoid necrosis in both Brattleboro and Long-Evans rats. 3. The levels of PRA and AII in the malignant hypertensive Brattleboro rats were not different from those in Long-Evans rats with malignant hypertension. 4. No compensation by the renin-angiotensin system therefore could be demonstrated for the lack of vasopressin in malignant hypertensive Brattleboro rats. 5. Vasopressin does not appear to be essential as a pressor hormone in the development of malignant renal hypertension and fibrinoid can occur in the absence of vasopressin.
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PMID:Vascular lesions and angiotensin in malignant hypertension in the absence of vasopressin. 675 78

We have studied microvascular reactivity to vasopressin alone and in combination with norepinephrine in young (6- to 8-week-old) spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) controls. Closed-circuit TV microscopy was used to quantify the in vivo diameter responses of small arterioles (17 to 26 mu) to vasopressin (1.25 X 10(-8) to 3.75 X 10(-7) M) injected intraarterially alone and with simultaneous topical suffusion of a subthreshold concentration of norepinephrine in the cremaster muscle microcirculation. Percent decrease in luminal diameter was integrated over a 30-second period to obtain log concentration response curves. The vasoconstrictor response to vasopressin was concentration-dependent in both groups (p less than 0.001). A significant increase in reactivity to vasopressin alone was exhibited by the SHR arterioles compared to the WKY vessels (p less than 0.02). Maximum constriction was 55% higher in the SHR (p less than 0.04). The SHR also demonstrated a greater sensitivity to vasopressin (p less than 0.02). Vasopressin-induced vasoconstriction was potentiated by norepinephrine in the SHR, demonstrated by the significant shift of the curve up and to the left of the SHR response curve to vasopressin alone (p less than 0.01). The maximum response was 38% greater (p less than 0.02). Sensitivity was significantly enhanced (p less than 0.01). Additionally, the presence of norepinephrine stimulated a three-fold greater incidence of complete closure. In contrast to SHR results, topical suffusion of norepinephrine did not significantly alter the reactivity of the WKY arterioles to vasopressin-induced constriction. Our results support a role for vasopressin as a potential vasoconstrictor in the developing stage of SHR hypertension which may be modulated by norepinephrine and thus contribute to the elevated total peripheral resistance observed.
Hypertension
PMID:Norepinephrine-induced potentiation of arginine vasopressin reactivity in arterioles of the spontaneously hypertensive rat. 684 Aug 20

1. In unanaesthetized sheep, transitory hypertension caused by intravenous angiotensin II and angiotensin III is not associated with a progressive increase in pulse interval, while hypertension caused by intravenous vasopressin produces a progressive increase in pulse interval. 2. Experiments in anaesthetized dogs showed that the three peptides do not alter the sensitivity of the carotid sinus baroreceptors. When arterial pressure was increased by angiotensin II and III, cardiac vagal efferent discharge did not increase as much as it did when blood pressure was raised by intravenous phenylephine or inflation of an intra-aortic balloon--often vagal discharge did not increase at all, or even fell. Vasopressin on the other hand produced a sustained and marked increase in cardiac vagal efferent nerve activity; this was in excess of the increase evoked when other agents were used to raise blood pressure. 3. Thus the three peptides can centrally modulate vagal control of heart rate.
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PMID:The effects of vasoactive peptides on the carotid cardiac baroreflex. 695

The contribution of vasopressin to the hypertensive process has been examined in a number of models of hypertension. Vasopressin is essential for the production of DOC-salt hypertension in the rat, It is likely that vasopressin is required in the early stages of this model of hypertension for its antidiuretic activity and contributes to the later stages of the hypertension as a pressor agent. Vasopressin secretion is increased in SHR, but there may be some differences between the SHR and stroke-prone SHR strains. The pressor action of vasopressin appears to be important in the stroke-prone SHR with well-established hypertension, but not in the young SHR. Vasopressin secretion is greater in Dahl S rats on a high salt diet than in similarly treated R rats. Blockade of vasopressin's pressor activity failed to lower blood pressure in these S rats, unless they were pretreated with captopril. There is insufficient information to determine whether vasopressin has a role in the hypertension in NZGH rats. Vasopressin appears to function as a pressor agent in some, but not all, rats with two-kidney, one clip hypertension. Although vasopressin is not essential for the production of one-kidney, one clip hypertension, it apparently contributes to the hypertension by virtue of its antidiuretic activity. Vasopressin secretion is elevated in partial nephrectomy-salt hypertension, and here, too, it is needed for its antidiuretic action. The question of whether vasopressin secretion is elevated in human essential hypertension is controversial, and its role remains to be determined.
Hypertension
PMID:Contribution of vasopressin to hypertension. 704 34

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).
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PMID:Vasopressin in the cerebrospinal fluid of patients with normal pressure hydrocephalus and benign intracranial hypertension. 711 92

An anteroventral third ventricle (AV3V) lesion in the brain prevents several forms of experimental hypertension. The present experiment was designed to determine whether the AV3V lesion prevents NaCl-induced hypertension in Dahl salt-sensitive (S) rats and whether attenuation of vasopressin release reported in lesioned rats contributes to the protective effect of the AV3V lesion against hypertension. After the AV3V lesion Dahl S rats received daily injections of either vasopressin (pitressin tannate, 500 mU/kg) or vehicle during 10 wk of 8% high-NaCl diet. Sham-lesioned rats served as controls. The blood pressure in sham-lesioned rats receiving vehicle was 189 mmHg after 10 wk of high-NaCl diet. Lesioned rats given vehicle showed a significantly smaller increase in blood pressure than sham-lesioned rats (P less than 0.001), the blood pressure averaging 161 mmHg at 10 wk. Lesioned rats given vasopressin also showed a smaller increase in blood pressure than sham-lesioned rats (P less than 0.05), but the final blood pressure averaged 176 mmHg and was significantly higher than that of lesioned rats given vehicle (P less than 0.025). Vasopressin injections corrected the hypernatremia in lesioned rats. In another experiment the effect of the AV3V lesion on the renal papillary plasma flow (RPPF) in Dahl S rats was studied. Dahl S rats have a lower RPPF than Dahl salt-resistant (R) rats even on a low-NaCl intake. The AV3V lesion increased the RPPF by 14% in S rats (P less than 0.025). These findings suggest that NaCl-induced hypertension in Dahl S rats requires the integrity of the AV3V region for its full expression, and the ability of the AV3V lesion to attenuate the NaCl-induced hypertension in Dahl S rats is partly related to the attenuation of vasopressin release. Moreover, the AV3V lesion partly corrected one of the characteristic features of Dahl S rats, the reduction in RPPF, when compared with Dahl R rats, with both strains on a low-NaCl intake.
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PMID:Effect of an anteroventral third ventricle lesion on NaCl hypertension in Dahl salt-sensitive rats. 712 69

Norepinephrine and epinephrine concentrations in the caudal and rostral part of the nucleus tractus solitarii (NTS) and in locus coeruleus (LC) of Sabra hypertension prone (SBH) rats are 2-4-fold higher than in the parent Sabra (SB) strain; SB rats have higher concentrations than the Sabra hypertension resistant (SBN) rats. Dopamine concentrations were higher in SBH as compared to SB and SBN rats only in the caudal NTS. Vasopressin concentrations in the NTS of SBH were 3-fold higher than the levels found in SB or SBN rats. These data suggest that catecholamines and vasopressin in specific brainstem nuclei are involved in either the pathogenesis or central response to hypertension in SBH rats.
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PMID:Catecholamines and vasopressin in hindbrain nuclei of hypertension prone and resistant rats. 717 1


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