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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Traditionally, arterial stenoses have been assumed to be inflexible, static obstructive lesions that could not acutely change their configuration or cross-sectional area. However, recent clinical and experimental observations have shown that coronary arterial stenoses can respond to vasoconstriction and intraluminal pressure changes. This experimental study evaluated whether similar dynamic changes could occur in a carotid artery stenosis. The effects of dilation distal to a circumferential snare were examined in 6 mongrel dogs. To eliminate collateral flow, the distal carotid artery was occluded and blood flow diverted through a 16 or 20 gauge needle. With no stenosis, distal dilation increased flow from 29.0 +/- 2.0 to 90.1 +/- 3.8 ml/min, (p less than 0.01). With moderate stenosis, the flow increase (25.5 +/- 1.3 to 56.4 +/- 3.7 ml/min, p less than 0.01 following dilation was attenuated. With severe stenosis, flow paradoxically decreased (20.4 +/- 1.0 to 11.4 +/- 1.0 ml/min, (p less than 0.01). This flow decrease was associated with a large stenotic resistance increase (2.13 +/- 0.51 to 18.93 +/- 5.58 mm Hg/ml . min-1, (p less than 0.01). In eight additional experiments, an in vitro preparation was used to examine the effects of vasoconstriction on stenotic severity. Vasoconstriction, induced by ergonovine, methoxamine, angiotensin, or vasopressin, resulted in a significant flow decrease and stenotic resistance increase. Thus, both vasoconstriction and intraluminal pressure were shown to affect stenotic severity, and thereby influence blood flow. These data illustrate hemodynamic factors which may be important in patients with severe carotid artery stenosis.
Stroke
PMID:Effects of vasoconstriction and distal dilation on carotid stenoses in the dog. 683 52

The brain stem and neurohypophyseal content of arginine vasopressin and the brain stem content of oxytocin were measured by radioimmunoassay in 3-, 7-, and 22- to 28-week-old spontaneously hypertensive rats of the stroke-prone strain (SHRSP) and the values were compared to those measured in age-matched normotensive Wistar-Kyoto rats (WKY). When compared to WKY, the content of vasopressin in the brain stems of SHRSP was reduced in all three age-groups; in contrast, the neurohypophyseal contents of vasopressin in the two species were not significantly different at 3 and 7 weeks of age and the content was increased slightly in SHRSP at 22-28 weeks. Similar to the findings for vasopressin in the brain stem, the content of oxytocin in this tissue was reduced in SHRSP at 7 and 22-28 weeks of age. The results demonstrate that brain stem arginine vasopressin levels and neurohypophyseal arginine vasopressin levels may change differentially and that the age-related differences in the brain stem levels of arginine vasopressin and oxytocin in SHRSP and WKY are consistent with the possibility that these peptides may play a role in altering cardiovascular reflex activity.
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PMID:Vasopressin and oxytocin content are decreased in the brain stems of spontaneously hypertensive rats. 687 23

We measured hemodynamics and renal function in conscious dogs while partially obstructing blood flow at various sites within the thorax. Inflation of a balloon in the left atrium increased left atrial pressure (LAP) by 9 mmHg and caused a parallel increase in pulmonary arterial pressure (PAP); heart rate, arterial pressure, and total peripheral resistance increased; stroke volume and right atrial pressure decreased; and cardiac output remained unchanged. The increase in LAP was accompanied by a fourfold increase in urine flow and a threefold increase in sodium excretion. Plasma vasopressin (AVP) and renin activity (PRA) decreased. On the other hand, partial occlusion of the pulmonary veins or the main pulmonary artery produced similar increases in PAP without affecting LAP, systemic hemodynamics, renal function, or plasma AVP. Similarly, inflation of a balloon in the right atrium failed to alter renal function, plasma AVP, or PRA. Finally, constriction of the thoracic inferior vena cava decreased LAP and increased PRA. In summary, these data emphasize that inflation of a balloon in the left atrium of the conscious dog produces a composite response consisting of alterations in cardiovascular function, renal function, and circulating hormones. Moreover, our data indicate that the response is mediated by a reflex initiated from receptors located in the left atrium; we detected no evidence that receptors located in the pulmonary vasculature or right heart contribute to this response.
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PMID:Reflexes elicited by acute stretch of atrial vs. pulmonary receptors in conscious dogs. 704 67

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.
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PMID:Contribution of vasopressin to hypertension. 704 34

Serum osmolality and antidiuretic hormone (ADH) levels were determined for 17 patients with cerebral infarction, 4 with subarachnoid hemorrhage, and 12 controls. The ADH levels were elevated significantly in the stroke patients. Hyponatremia was not observed. Stroke patients are at risk for developing electrolyte disturbances; thus, fluid intake and electrolyte levels should be closely observed.
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PMID:Antidiuretic hormone levels in stroke patients. 723 33

Arginine-vasopressin (AVP) content was measured by radioimmunoassay in the plasma and brain of stroke-prone spontaneously hypertensive rats (SHRsp) and normotensive Wistar Kyoto (WKY) control rats. AVP was reduced in plasma, hypothalamus, amygdala, septum and brain stem of the hypertensive animals. In view of the possible sensitizing effect of vasopressin on the baroreceptor reflex, the reduction of this peptide in the brain stem could contribute to hypertension in SHRsp.
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PMID:Reduced content of vasopressin in the brain of spontaneously hypertensive as compared to normotensive rats. 725 7

1. Plasma concentration of arginine vasopressin, plasma osmolality and packed cell volume were measured in stroke-prone spontaneously hypertensive rats (SHRSP) and in normotensive Wistar-Kyoto (WKY) rats at different ages. 2. In young and in adolescent SHRSP, at 6, 9 and 12 weeks of age, plasma concentration of vasopressin was diminished as compared with age-matched WKY rats (P less than 0.01), whereas, in 18-week-old rats, the difference was not significant (P greater than 0.05). In contrast, in 24-week-old rats, plasma vasopressin was elevated as compared with WKY rats of the same age (P less than 0.01). 3. In none of the age groups did plasma osmolality differ between the two strains of rats, but in all groups packed cell volume in SHRSP was higher than in WKY rats. 4. During a 48 h period of dehydration, plasma vasopressin concentrations increased similarly in SHRSP and in WKY rats of 6 and 12 weeks of age respectively. 5. It is concluded that vasopressin does not contribute to the development of high blood pressure in SHRSP rats. The reduced plasma concentration of vasopressin may account for the decreased plasma and blood volume and the slightly elevated plasma sodium concentration observed in young SHRSP rats.
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PMID:Vasopressin in the plasma of stroke-prone spontaneously hypertensive rats. 726 51

Vascular resistance and reactivity were investigated in isolated, constant flow perfused kidneys of stroke-prone spontaneously hypertensive rats (SHRSP) and age- and sex-matched normotensive Wistar-Kyoto control rats (WKY rats). Stroke-prone spontaneously hypertensive rats were studied at 4 wk, 2 mo, and 4 mo of age representing different stages of development of hypertension. Resistance in maximally vasodilated vascular beds was greater and the pressure-flow relationship was significantly shifted to the left in kidneys of SHRSP as compared to WKY rats. Responses to norepinephrine, vasopressin, serotonin, and angiotensin II were enhanced in the renal vascular bed of SHRSP. Dose-response curves were shifted to the left, had steeper slopes, decreased thresholds, and increased maximal responses. With longer duration of hypertension, resistance increased, the slopes of the dose-response curves were steeper, and maximum responses greater. The higher resistance and enhanced reactivity in the renal vasculature of SHRSP, already demonstrable in the prehypertensive stage appear to be due to primary structural and functional alterations of the resistance vessels.
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PMID:Alterations in renal vascular resistance and reactivity in spontaneous hypertension of rats. 736 72

The mechanisms by which elevated levels of vasopressin (ADH) in man and animals cause serious myocardial dysfunction, evidenced by arrhythmias, reduction in cardiac output and coronary blood flow, are not settled. Experiments were conducted in 16 isolated working left ventricles to examine their metabolic and hemodynamic responses to the infusion of vasopressin and the combination of vasopressin and epinephrine. Contractile performance was evaluated by analysis of positive dP/dt, contractile element velocities, and ventricular work-curves using stroke work/end-diastolic pressure. Relaxation parameters, including negative dP/dt and the early diastolic relaxation time constant, were also studied. Coronary blood flow was reduced 22% or less by vasopressin while cardiac output was maintained at a constant level. Myocardial oxygen consumption, lactate and potassium balances were determined from arterial and coronary sinus concentrations. Vasopressin produced myocardial dysfunction indicated by decrements in contractile and relaxation indices, without evidence of global ischemia. Epinephrine restored the mechanical performance to normal without significant change in coronary blood flow, myocardial oxygen consumption, or lactate and potassium balance.
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PMID:Mechanisms of impaired cardiac function by vasopressin. 736 15

In patients with essential hypertension the blood antidiuretic activity was studied in relation to the haemodynamics. It was found that the blood antidiuretic activity increased in parallel with the rise in the total peripheral resistance, and with the decreases in the blood and plasma volumes, stroke volume, and end-diastolic heart volume. The role of antidiuretic hormone in the regulation of haemodynamics in hypertensive patients is discussed.
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PMID:Blood antidiuretic activity and selected haemodynamic indicators in patients with essential hypertension. 739 48


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