Effects of chronic central administration of losartan on the cardiovascular and hormonal responses to hemorrhage in conscious rats

Yang, Eun-Kyoung; Lee, Won-jung; Park, Yoon-yub; Ahn, Dongbin; Park, Jaesik; Kim, Hyeong-Jin

doi:10.1016/s0167-0115(96)00114-0

Cited by 15 publications

(9 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition to the effect of circulating ANG II on the renal renin synthesis and secretion, ANG II in the brain may also have an inhibitory effect on the renin release. The central administration of ANG II decreases renin secretion, and the central administration of losartan increases renin secretion (387,573,942,968). This effect on renal renin secretion is likely due to a reduction in the renal sympathetic nerve activity (574).…”

Section: Physiology Of Kidney Reninmentioning

confidence: 99%

Physiology of Kidney Renin

Castrop

Höcherl

Kurtz

et al. 2010

Physiological Reviews

232

277

View full text Add to dashboard Cite

The protease renin is the key enzyme of the renin-angiotensin-aldosterone cascade, which is relevant under both physiological and pathophysiological settings. The kidney is the only organ capable of releasing enzymatically active renin. Although the characteristic juxtaglomerular position is the best known site of renin generation, renin-producing cells in the kidney can vary in number and localization. (Pro)renin gene transcription in these cells is controlled by a number of transcription factors, among which CREB is the best characterized. Pro-renin is stored in vesicles, activated to renin, and then released upon demand. The release of renin is under the control of the cAMP (stimulatory) and Ca2+(inhibitory) signaling pathways. Meanwhile, a great number of intrarenally generated or systemically acting factors have been identified that control the renin secretion directly at the level of renin-producing cells, by activating either of the signaling pathways mentioned above. The broad spectrum of biological actions of (pro)renin is mediated by receptors for (pro)renin, angiotensin II and angiotensin-( 1 – 7 ).

show abstract

Section: Physiology Of Kidney Reninmentioning

confidence: 99%

Physiology of Kidney Renin

Castrop

Höcherl

Kurtz

et al. 2010

Physiological Reviews

232

277

View full text Add to dashboard Cite

show abstract

“…2,[17][18][19] Brain angiotensin also enhances adrenergic tone by central activation and facilitation of sympathetic transmission 20 and increasing catecholamine turnover in sympathetic brain nuclei. 21 Since central blockade of AT 1 receptor with losartan significantly attenuates the pressor response to sympathetic stimulation-induced haemorrhage, 22 immobilization stress 23 and footshocks, 5 a role for brain AT 1 receptors has been suggested in the facilitation of noradrenergic transmission and pressor response to stress. Indeed, in various brain nuclei relevant to cardiovascular control, AT 1 receptor activation regulates uptake, synthesis and release of noradrenaline and dopamine.…”

Section: Introductionmentioning

confidence: 99%

Role of bradykinins and nitric oxide in the AT2 receptor-mediated hypotension

et al. 2000

View full text Add to dashboard Cite

Footshocks increases mean arterial pressure and heart rate. Systemic or intracerebroventricular (IVT) administration of losartan, a specific angiotensin AT 1 receptor antagonist, not only inhibited the pressor response to footshocks but resulted in vasodepression. Peripheral or IVT administration of PD 123319, a specific angiotensin AT 2 receptor antagonist, did not alter the haemodynamic response to footshocks. However, simultaneous blockade of angiotensin AT 1 and AT 2 receptors by combined systemic or central administration of losartan and PD 12319, eliminated the vasodepressor response to footshocks unmasked in losartan pretreated rats. Our data suggest that activation of peripheral or brain angiotensin AT 2 receptor mediated the vasodepressor response to footshocks in the presence

show abstract

“…By contrast, there was only a five-fold increase in plasma norepinephrine. By comparison, other stimuli to adrenal epinephrine release in the intact rat, such as haemorrhagic hypotension or exercise, elicit much lower arterial concentrations, in the range of 2.2-5.5 nmol/l, respectively [33,34]. Both the increase in plasma epinephrine and norepinephrine as well as the acute increases in blood pressure and heart rate evoked by b-FXIIa injection were absent in Brown Norway adrenodemedullated rats, and also in plasma kininogen-deficient BNK rats, indicating that both the adrenal medullae and an intact plasma KKS are required for this response to occur (Fig.…”

Section: Discussionmentioning

confidence: 84%

Adrenomedullary catecholamine, pressor and chronotropic responses to human coagulation β-FXIIa mediated by endogenous kinins

Amfilochiadis

Backx

Floras

2008

Journal of Hypertension

View full text Add to dashboard Cite

The pressor and chronotropic responses to beta-FXIIa in this bioassay preparation are mediated exclusively through adrenal catecholamine release, and require plasma kininogens for their full expression. These observations suggest that interaction between the coagulation, kallikrein-kinin and sympatho-adrenal systems can exert important pressor effects in the absence of counterregulatory autonomic reflexes.

show abstract

Effects of chronic central administration of losartan on the cardiovascular and hormonal responses to hemorrhage in conscious rats

Cited by 15 publications

References 21 publications

Physiology of Kidney Renin

Physiology of Kidney Renin

Role of bradykinins and nitric oxide in the AT2 receptor-mediated hypotension

Adrenomedullary catecholamine, pressor and chronotropic responses to human coagulation β-FXIIa mediated by endogenous kinins

Contact Info

Product

Resources

About