RENIN SECRETION IN CONSCIOUS LYON HYPERTENSIVE RATS

Citation
S. Bertolino et al., RENIN SECRETION IN CONSCIOUS LYON HYPERTENSIVE RATS, American journal of physiology. Regulatory, integrative and comparative physiology, 40(5), 1996, pp. 1199-1204
Citations number
34
Categorie Soggetti
Physiology
ISSN journal
03636119
Volume
40
Issue
5
Year of publication
1996
Pages
1199 - 1204
Database
ISI
SICI code
0363-6119(1996)40:5<1199:RSICLH>2.0.ZU;2-V
Abstract
To characterize the renin secretory profile in Lyon hypertensive (LH) rats, renin responses to reductions of arterial pressure and beta-adre noceptor stimulation were assessed in conscious unrestrained LH (n = 1 3) and Lyon normotensive (LN, n = 14) rats under normal-salt diet. Mea n arterial pressure (MAP) in the infrarenal aorta was recorded beat to beat for 3 h. Then, plasma renin concentration (PRC) was measured 1) in basal conditions, 2) during 10-mmHg stepwise reductions of MAP down to 60 mmHg using a chronically implanted aortic inflatable cuff, and 3) during isoprenaline infusion (62.5, 125, and 250 ng . kg(-1). min(- 1) iv). Compared with LN, LH rats had an elevated MAP (146 +/- 3 vs. 1 11 +/- 1 mmHg, P < 0.001) and decreased PRC [4.2 +/- 0.6 vs. 8.2 +/- 0 .8 ng angiotensin (ANG) I . ml(-1). h(-1), P < 0.001] and kidney renin content (216 +/- 14 vs. 1,149 +/- 103 mu g ANG I . h(-1). g(-1), P < 0.001). Pressure-dependent renin release occurred below 90 mmHg in LN rats and below 80 mmHg in LH rats, and its sensitivity in the low-pres sure range did not differ between strains. Isoprenaline-induced increa ses in PRC were weaker (P <( 0.01) in LH than in LN rats. In additiona l LH and LN rats (n = 6-8), acute ANG II AT(1)-receptor blockade with losartan (20 mg/kg, followed by 10 mg . kg(-1). h(-1) iv for 2 h) indu ced lesser (P < 0.001) PRC increases in LH than in LN rats. Renin resp onses to isoprenaline remained blunted (P < 0.01) during losartan infu sion in LH rats. We conclude that, in LH rats, renin secretion is inde pendent of MAP in the range of its spontaneous variations and is poorl y responsive to beta-adrenoceptor stimulation, the alteration of which cannot be explained by an enhanced feedback inhibition by ANG II.