摘要:

The role of aradrenergic receptor stimulation in the regulation of systemic vascular capacity and venous return, a major determinant of cardiac output, is not well understood. With the influence of the central nervous system isolated from the systemic circulation, the direct peripheral vascular effects of two specific, chemically distinct α2-adrenergk receptor agonists, UK 14,304 and BHT 920, were investigated in 19 dogs on total cardiopulmonary bypass with constant arterial perfusion and central venous pressure. Five-minute intra-arterial infusions of UK 14,304 (200 μ/min) resulted in increased arterial resistance (mean arterial pressure increased 18 ± 4 [SEM] mm Hg;p< 0.01) and a decrease hi systemic vascular capacity (81 ± 20 ml;p< 0.01). This decrease in systemic vascular capacity appears to result from vasoconstriction, since there was no decrease in transhepatic resistance to portal flow and no significant change in hepatic vein flow to suggest redistribution of arterial blood flow. Yohimbine abolished both the arterial and systemic capacity effects, whereas prazosin did not. Intra-arterial administration of B-HT 920 (200 &thetas;g/min) in five dogs produced similar changes in arterial resistance and systemic capacity. These findings provide direct evidence for β2-adrenergic control, not only of arterial resistance but also of systemic vascular capacity, which in the intact nnlmnl would increase venous return to the heart.

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

In conscious spontaneously hypertensive rats (SHR), 2, 3, 6, 9, 12, and 16 months of age, the blockade of autonomic ganglia (with chlorisondamine) or postjunctional α1-adrenergic receptors (with prazosin) or the depletion of peripheral norepinephrine stores (with syrosingopine), in contrast to the blockade of aradrenergic receptors (with yohlmbine, rauwolscine), produced a sustained decrease in the directly measured mean tail artery blood pressure. In 3- to 9-month-old SHR, the fall in blood pressure after prazosin pretreatment was significantly smaller than that after chlorisondamine or syrosingopine pretreatment. In ganglion-blocked SHR, prazosin decreased blood pressure only when this parameter had been elevated by an intra-arterial infusion of epinephrine or norepinephrine. In contrast, under the same experimental conditions, yohimbine or rauwolscine administration failed to modify the pressor effects of either phenylephrine or epinephrine but partially reduced those of norepinephrine and, unlike prazosin, strongly antagonized those of B-HT 920. In either intact or ganglion-blocked SHR, a 30-minute intra-arterial infusion of diltiazem at 100.0, but not 25.0, μg/kg/min significantly decreased baseline mean tail artery blood pressure. In ganglionblocked SHR, the smaller dose of diltiazem antagonized by 40 and 80% the pressor effects of norepinephrine and B-HT 920, respectively, but failed to change the vasoconstrictor responses of phenylephrine, epinephrine, or vasopressln, which were, however, reduced by the higher dose of diltiazem. These results indicate that, in conscious adult SHR, norepinephrine released by peripheral sympathetic nervous terminals and humoral ly borne epinephrine stimulate almost exclusively postjunctional α1-adrenergic receptors. The latter findings may account for the lack of blood pressurelowering effects of the studied calcium antagonists at doses that effectively antagonize α2-adrenergic receptor-mediated vasoconstriction in conscious SHR.

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

The tail-cuff methods for measuring systolic blood pressure in the rat usually require preheating of the animal to obtain recordable pulse signals. To find a more sensitive method, we applied the principle of differentiated impedance (dZ/dt) to the tail-cuff measurement of systolic blood pressure. We obtained clear pulse signals from the tail in awake rats without preheating the animals, and the systolic blood pressure obtained by this method had an excellent correlation with the directly measured femoral artery pressure (correlation coefficient=0.98). Heating the animals at 40°C for 5 minutes increased systolic blood pressure by a mean of 6 mm Hg as compared with that determined at the ambient temperature of 21 to 24°C. Mean systolic blood pressure in young female diabetic rats was 122 ± 3 mm Hg, which was significantly higher than the 111 ± 2 mm Hg of normal rats. It is concluded that the technique of electrical impedance as applied to the tail-cuff method is simple and highly sensitive and is suitable for measurement of tail systolic blood pressure in awake rats without preheating.

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

In spontaneously hypertensive rats (SHR), the progression (or absence of regression) of cardiac hypertrophy despite adequate blood pressure (BP) control by arterial vasodilators has been attributed to increased cardiac sympathetic activity. We evaluated changes in indices of general and cardiac sympathetic tone in relation to changes in cardiac anatomy during treatment of normotensive rats and SHR with hydralazine, 120 mg/L, or minoxidil, 120 mg/L of drinking water. In SHR, both vasodilators reduced BP rapidly and consistently. Significant increases in heart rate and plasma norepinephrine were observed only in the initial 2 days of arterial vasodilator treatment. After 5 weeks of treatment, marked increases in left and right ventricular sympathetic activity (as assessed by norepinephrine turnover rates) were present, but no increase was seen in heart rate and plasma norepinephrine. Intravascular volume expansion was observed on Day 14 of minoxidil and Day 35 of hydralazine treatment. Prolonged treatment with minoxidil induced significant increases in left ventricular internal diameter, as well as in left and right ventricular weights, but not in the wall thickness of the left ventricle. Treatment with hydralazine did not affect left ventricular weight and caused a small increase in the weight of the right ventricle. In normotensive rats, both vasodilators initially decreased BP, but tolerance developed within 1 to 2 weeks of treatment. Plasma norepinephrine and heart rate showed increases only at Day 1 of either treatment, whereas cardiac sympathetic hyperactivity persisted at 2 and 5 weeks of treatment. Changes in cardiac anatomy were qualitatively similar to those observed in SHR. We conclude that, during treatment of normotensive rats and SHR with arterial vasodilators, cardiac sympathetic hyperactivity persists and may be involved in the cardiac effects of arterial vasodilators. However, other mechanisms, such as chronic cardiac volume overload, may also play an important role, particularly with minoxidil.

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

Pyridoxal phosphate Is the coenzyme of various decarboxylases involved in the formation of monoamlne neurotransmitters such as γ-aminobutyric acid, serotonin, dopamine, and norepinephrine. Adult male Sprague-Dawiey rats placed on a pyridoxine-deficient diet for 8 weeks showed significant hypertension compared with pyridoxJne-supplemented controls. Hypothalamic contents of pyridoxal phosphate, γ-aminobutyric acid, and serotonin in the pyridoxine-deficient rats were significantly lower than those in pyridoxine-supplemented controls. Hypertension was associated with sympathetic stimulation. Treatment of pyridoxine-deficient rats with a single dose of pyridoxine (10 mg/kg body weight) reversed the blood pressure to normal levels within 24 hours, with concomitant restorations of hypothalamic serotonin and γ-aminobutyric acid as well as the return of plasma norepinephrine and epinephrine to normal levels. Also, pyridoxine treatment reversed the hypothalamic hypothyroidism observed in pyridoxine-deficient rats. These results indicate an association between pyridoxine deficiency and sympathetic stimulation leading to hypertension.

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID

摘要:

The cellular mechanism of the action of atrial natriuretic factor (ANF) is thought to involve activation of guanylate cyclase. Increasing evidence shows a direct tubular effect of ANF. Part of the ANF-induced diuresis has been suggested to be due to inhibition of the action of arginine vasopressin (AVP) in the cortical collecting tubule. In this study we investigated the effect of ANF on cyclic nucleotide production in primary cultures of cortical collecting tubule cells immunodissected with a monoclonal antibody. ANF caused a dose-dependent stimulation in cyclic guanosine 3′,5′-monophosphate (cGMP) production; the half-maximal stimulation was observed at 1 nM of ANF. ANF (0.01–100 nM) had no effect on cyclic adenosine 3,5-monophosphate (cAMP) accumulation in cortical collecting tubule cultures. AVP caused a dose-dependent increase in cAMP production, and this effect was not altered by the simultaneous addition of ANF (100 nM). Similarly, ANF-induced cGMP stimulation was not influenced by AVP (10 nM). We conclude that 1) ANF has a direct stimulatory action on cGMP production by cultured cortical collecting tubule cells and 2) any interaction between ANF and AVP is likely to occur at steps distal to cyclic nucleotide formation.

ISSN:0194-911X    

出版商:OVID    

年代:1988

数据来源: OVID