Publications by authors named "Cowley A"

We examined the effects of physiologic infusions of arginine vasopressin (AVP) on cardiovascular hemodynamics and on reflex responses initiated by decreasing cardiopulmonary baroreceptor stimulation (with lower body negative pressure) in 10 healthy, captopril-pretreated young men (19-27 yr). Their responses were compared with those of four volunteers given isosmotic infusion. Heart rate, stroke volume, blood pressure, and forearm blood flow were measured by electrocardiography, impedance cardiography, radial artery cannulation, and strain gauge plethysmography.

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The effects of chronic combined administration of angiotensin II, norepinephrine, aldosterone, and arginine vasopressin were compared with the response to each of these hormones administered alone. The studies were performed in dogs to determine the extent to which moderately inappropriate elevations of these hormones could enhance each other's ability to produce chronic hypertension and influence Na and water homeostasis. Blood pressure sensitivity to Na intake was also evaluated by infusing the hormones for 11 days at normal levels of Na intake followed by 11 days at high Na intake with ad libitum drinking.

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The effects of aspirin and dazoxiben were determined on platelet behaviour in platelet-rich plasma (PRP) from 20 volunteers. Dazoxiben prevented aggregation and the release reaction induced by arachidonic acid (AA) in nine of the samples; in the other eleven aggregation and the release reaction still occurred. Aspirin always prevented aggregation and release but higher concentrations were needed in some of the samples of PRP than with others.

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The effects of chronic (4 days) arginine vasopressin (AVP) infusion were studied in two separate groups of animals: normal Na-restricted dogs with intact renal nerves (n = 8) and renal-denervated Na-restricted dogs (n = 5). Volume expansion during AVP infusion was prevented in these studies with a sensitive servo-controlled cage-scale system. With intravenous AVP infusion (0.

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Forearm venous tone was measured in two groups of pregnant women: one group with pregnancy-induced hypertension and the other group with normal blood pressure. The women with pregnancy-induced hypertension were venoconstricted in the forearm (P less than 0.01) compared with the pregnant women with normal blood pressure.

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To investigate the peripheral circulatory and respiratory abnormalities which occur in patients with heart failure, forearm and calf blood flow were measured before and after upright exercise, and respiratory gas exchange was measured during exercise in 26 patients with severe heart failure. Compared with a group of normal subjects the patients had reduced limb blood flow at rest and the response of limb blood flow to upright exercise was also abnormal. The increase in calf blood flow after exercise and the reduction in blood flow in the non-exercising forearm were both smaller in patients than in controls.

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Three groups of dogs were studied to determine to what extent the suppression of plasma renin activity (PRA), natriuresis, and hyponatremia, seen with chronic elevations of plasma vasopressin (AVP), were caused by volume expansion or some other more direct actions of AVP. The dogs of group 1 (n = 7) were infused with AVP (0.36 ng/kg/min, i.

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Arginine vasopressin (AVP) is known to produce increases in total peripheral resistance (TPR) and mean arterial pressure (MAP) and decreases in heart rate (HR), cardiac output (CO), and plasma renin activity (PRA). Some recent observations with AVP and synthetic analogues have suggested that under certain conditions, AVP can induce cardiovascular and reninsecretory responses in the opposite directions. To characterize the receptors mediating these responses, the effects of AVP, oxytocin, and synthetic neurohypophyseal analogues with specific antidiuretic, vasoconstrictor, or oxytocic activities were studied in conscious dogs.

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Adrenocorticotropin (ACTH), cortisol, and vasopressin responses to clamped decreases in blood pressure (MAP) and to ovine corticotropin-releasing factor (CRF) infusion (20 ng X kg-1 X min-1) in intact and neurohypophysectomized (NHX) conscious dogs were examined. Mean arterial blood pressure was decreased 28 mmHg by a controlled infusion of sodium nitroprusside. Hypotension induced large increases in ACTH (peak 164 +/- 25 pg/ml), cortisol (peak 12.

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The role of the baroreceptor mechanism in determining the relationship between fluid volume and arterial pressure is not clear. Therefore, the effects of the baroreflex on the arterial pressure and fluid volume of conscious, anephric dogs were studied after a sustained 10% increase in blood volume. The animals were equipped with long-term indwelling arterial and venous catheters, and arterial pressure was monitored 24 hours a day.

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Previous studies have shown that in normal humans plasma arginine vasopressin (AVP) does not increase in response to unloading of cardiopulmonary and sinoaortic baroreceptors produced by lower body negative pressure (LBNP) unless hypotension occurs. To assess whether prior osmotic stimulation of AVP might bring out latent sensitivity to nonosmotic control mechanisms in humans we studied the response of plasma AVP to graded LBNP after a 105-min infusion of 5% saline in a group of eight normal individuals. During the infusion and before LBNP, serum osmolality increased from 288 +/- 9 to 300 +/- 10 mosmol/kg, and plasma AVP increased from 4.

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The relationships between arterial pressure (BP) and plasma vasopressin levels, plasma renin activity, and other variables were determined in 96 untreated essential hypertensive men (146/100 mm Hg) and women (153/102 mm Hg) whose average age was 44 years, 80 normal men and women (121/79 mm Hg; mean age, 47 +/- 2 years), and 40 subjects defined as borderline hypertensive. An analysis of variance indicated significant sex differences in the population. Levels of plasma vasopressin were significantly elevated in hypertensive men, with 26% (high plasma vasopressin hypertensive) exhibiting levels greater than 2 SD of the normal mean, and multivariate regression analysis indicated a significant positive correlation between plasma vasopressin levels and systolic and diastolic blood pressure.

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To evaluate the possible role of prostaglandins in exercise-induced changes in blood pressure and limb blood flow we have compared the effects of aspirin and indomethacin in a double-blind placebo controlled study in a group of normal volunteers. Nine men undertook treadmill exercise after pretreatment with placebo, aspirin and indomethacin. Indomethacin caused a greater increase in systolic blood pressure during exercise than aspirin (p less than 0.

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PGI2 and ZK 36374 were each infused into volunteers and the effects on forearm blood flow and on platelet behaviour were determined. Infusions of PGI2 or ZK 36374 did not alter resting forearm blood flow but both agents reduced the extent of the vasoconstriction that occurred in response to cold. ZK 36374 appeared to be a much more potent inhibitor of platelet behaviour than PGI2 when blood was taken while the infusions were in progress, but the effects of both agents were no longer evident one hour after the infusions were terminated.

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The renal responses to changes in perfusion pressure (RPP) were studied in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) to determine whether an abnormality in the pressure-diuresis phenomenon could be involved in the resetting of kidney function in hypertension. Differences in the neural and endocrine background to the kidneys were minimized by denervating the kidney and by holding plasma vasopressin, aldosterone, corticosterone, and norepinephrine levels constant by intravenous infusion. In WKY, increasing renal perfusion pressure 54 mmHg, from 103 to 157 mmHg, produced a ninefold increase in urine flow and sodium excretion with no measurable change in renal blood flow (RBF) or glomerular filtration rate (GFR).

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The acute relationships between the urinary excretion of sodium and water and renal perfusion pressure were characterized in the rat using a new in vivo model of pressure diuresis. Neural and hormonal influences on the kidney were held constant by denervating the kidney and by maintaining fixed high plasma levels of vasopressin, aldosterone, corticosterone, and norepinephrine levels by intravenous infusion. Renal perfusion pressure (RPP) was varied above and below control using specially designed aortic clamps.

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The effect of dazoxiben, a thromboxane synthetase inhibitor, on cold-induced forearm vasoconstriction was determined in two groups of human volunteers, those in whom dazoxiben abolished the platelet aggregation and release reaction induced by sodium arachidonate (group I) and those in whom it did not (group II). Dazoxiben abolished cold-induced forearm vasoconstriction in group I volunteers but not in those of group II. These results imply a correlation between platelet behaviour and cold-induced changes in vascular tone.

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The pharmacokinetics and cardiovascular effects of a new vasodilator, BTS 49465 (7-fluoro-1-methyl-3-methylsulphinyl-4-quinolone) were evaluated in a double-blind placebo-controlled manner in a group of normal male volunteers. Forearm vascular resistance and forearm venous tone were measured by venous occlusion plethysmography using mercury-in-rubber strain gauges, supine, and in response to lower body negative pressure. Systemic arterial pressure was also measured.

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Studies were performed to ascertain the extent to which arterial blood pressure, and fluid and electrolyte changes seen with chronic elevations of plasma vasopressin (AVP) were caused by volume expansion or some other more direct cardiovascular or neural interactions of AVP. Group 1 (n = 7) dogs were infused with AVP (0.36 ng/kg/min) while total body weight and volume were maintained at a constant level by the use of an electronically controlled servocontrol system.

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Limb blood flow and respiratory function were compared in ten patients with severe heart failure inadequately controlled by diuretics and normal control subjects matched for age and sex. Both forearm and calf blood flow, at rest and after exercise, were lower in the patients than in the control subjects. Oxygen consumption during submaximal exercise was also lower in the patients and minute ventilation was higher.

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Drugs that cause vasodilatation tend to inhibit platelet behaviour whereas compounds that cause vasoconstriction stimulate platelet behaviour. Thus there appears to be a similarity between platelet behaviour and vascular tone. To investigate this relationship we have compared the maximum vasoconstrictor response in the forearm induced by cold stimulation with some aspects of platelet behaviour.

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