摘要:

We sought to determine the role in control of arterial pressure (AP) of the caudal ventrolateral medulla (CVL), a region containing noradrenergic neurons of the A1 group. Electrical stimulation of the A1 area in anaesthetized rats elicits a fall of AP and heart rate at low, but not high, stimulus frequencies. Electrolytic lesions of the A1 area produce fulminating hypertension and a 13-fold increase in plasma arginine vasopressin (AVP). A1-hypertension is attenuated by treatment with an AVP antagonist and is also diminished in rats of the Brattleboro strain. After AVP blockade, the residual hypertension is abolished by treatment with ganglionic or alpha adrenergic blockers, but not by adrenalectomy. We conclude that the region of the CVL containing the A1 noradrenergic cells tonically inhibits the discharge of sympathetic nerve activity as well as the release of AVP from the pituitary.

ISSN:0263-6352    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

In control dogs and those made hypertensive for 1 and 8 months by partially occluding a renal artery, contractile responses of mesenteric artery strips to adrenergic nerve stimulation and to norepinephrine, plasma renin activity and vascular angiotensin converting enzyme (ACE) activity were compared. Contractile responses to norepinephrine were potentiated in the artery strips from 8-month-hypertensive dogs; however, the response to electrical stimulation of adrenergic nerves was not influenced. Contractions induced by the nerve stimulation were potentiated by a low concentration (2 x 10-10mol/l) of angiotensin (ANG) II; the potentiating effect was enhanced in 8-month-hypertensive dog arteries.3H-overflow evoked by adrenergic nerve stimulation was increased by ANG II to a greater extent in superfused mesenteric artery strips obtained from hypertensive (8-month) dogs, previously soaked in3H-norepinephrine. Angiotensin convertingi enzyme activity was markedly greater in 8-month-hypertensive dog mesenteric arteries than in normotensive dog arteries. It may be concluded that the hypertension is maintained by increased sensitivity of post-synaptic α1-adrenoceptors and pre-synaptic ANG receptors and increased vascular ACE activity, possibly promoting the production of ANG II in the vascular wall.

ISSN:0263-6352    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

This study investigated the mechanism underlying the exaggerated natriuresis seen in patients with essential hypertension. The study used the lithium clearance method, which permits accurate determination of both proximal and distal sodium reabsorption in man. One litre of isotonic sodium chloride, intravenously (i.v.), produced a significant increase in sodium excretion in patients with essential hypertension, both during and after the infusion. This increase in sodium excretion was accompanied by a significant increase in the clearance of lithium, indicating an increased output of isotonic fluid from the proximal tubules. The calculated distal reabsorption of sodium increased during the natriuresis. In the normotensive controls, sodium excretion increased only after the infusion of 1 I isotonic saline. This was accompanied by a modest increase in absolute distal sodium reabsorption. However, when the amount of saline was increased to 2 I, similar changes to those seen in hypertensives given 1 I of saline occurred in normotensive subjects. Furthermore, chronic antihypertensive treatment abolished the phenomenon of exaggerated natriuresis.It is concluded that the exaggerated natriuresis represents the normal response to sodium loading being reset to a lower level. This resetting may be a secondary consequence of the high blood pressure, since lowering the pressure abolishes the phenomenon.

ISSN:0263-6352    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

The function of the renin-angiotensin system (RAS) is influenced by changes in sodium balance and angiotensin II (ANG II) levels. In previous studies it has been difficult to assess the physiological effects on blood pressure homeostasis of different rates of ANG II infusion and of different levels of sodium in the diet. The present study examined the quantitative effects of ANG II in conscious dogs on low, normal and high sodium intake with the endogenous RAS blocked by continuous intravenous infusion of enalapril [MK-421,N-(1(S)-carbethoxy-3-phenyl propyl)-L-alanyl-L-proline maleate].Conscious dogs on three different sodium diets, low, normal and high (5,30 and 250 mmol/day), were infused continuously with enalapril, 4 mg/kg/day, and studied with superinfused ANG II at rates of 0,1,3, 6 and 12 ng/kg/min, each period lasting 1 week. Converting enzyme inhibitor (CEI) decreased mean arterial blood pressure (MAP) equally in dogs on low and normal sodium intake by 20 mmHg, but did not have a significant effect in dogs on high sodium intake. The initial infusion of ANG II at the lowest rate had a pronounced effect on MAP in dogs on normal and high sodium, but had no effect in the sodium depleted dogs. However, at the higher rates of infusion, the angiotensin increased the pressure, equally at all levels of sodium intake.All four dogs in the high sodium group developed circulatory difficulties at the 6 or 12 ng level of ANG II infusion; one suffered gastrointestinal haemorrhage, one developed congestive failure and in the other two the arterial pressure remained elevated by an average of 23 mmHg after removal of all drugs. At all levels of ANG II infusion, glomerular filtration rate (GFR) was about 20% less in the sodium depleted dogs than in dogs on normal and high sodium, and effective renal plasma flow (ERPF) was about 25% greater in the high sodium group than in the normal and sodium deficient dogs. Plasma renin activity (PRA) increased in all groups after CEI treatment; however, the increased activity was suppressed by much smaller rates of angiotensin infusion in sodium loaded dogs and in dogs on normal sodium than in the sodium depleted dogs. Plasma aldosterone increased significantly more at low infusion rates of ANG II in sodium depleted dogs than in the other two groups. The present study indicates that at low ANG II levels, vascular sensitivity to ANG II is reduced in the sodium depleted state, while adrenal sensitivity to ANG II is increased, compared with the sodium replete state. Also, ANG II infusion and high dietary sodium can have independent effects on both PRA and plasma aldosterone concentration.

ISSN:0263-6352    

出版商:OVID    

年代:1985

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1985

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1985

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1985

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1985

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1985

数据来源: OVID

ISSN:0263-6352    

出版商:OVID    

年代:1985

数据来源: OVID