Impaired baroreflex sensitivity and responses to angiotensin converting enzyme inhibitor in salt-induced hypertension and its prevention by dietary calcium supplement in Sprague-Dawley rats.
The role of renin-angiotensin system and baroreceptors in the pathogenesis and prevention of hypertension due to salt-loading and concurrent dietary calcium for 6 weeks in Sprague-Dawley rats were studied. Blood pressure measurements were done in anaesthetized animals while the activities of renin-angiotensin and parasympathetic nervous systems were determined by the effect of their inhibition on the arterial pressure and baroreflex sensitivity, via captopril infusion and vagotomy respectively. The sympathetic nervous system activity and its effect on baroreflex response were estimated by combined captopril infusion and vagotomy. There was elevation of mean arterial pressure (MAP) in salt-loaded rats (SR) relative to controls (NR) (140.5 +/- 2.18 vs 98.0 +/- 1.38 mmHg) without any significant effect on heart rate (HR) (406 +/- 8.58 vs 428 +/- 11.20 beats/min). Calcium supplement abolished the rise in MAP of salt-loaded-calcium-fed rats (SCaR) (102.8 +/- 2.30 mmHg) but led to reduction in their HR (389 +/- 10.21 beats/ min) relative to control. Renin-angiotensin system inhibition led to fall in MAP in all groups of rats with the greatest reduction observed in SR. Inhibition of parasympathetic effects resulted in elevation of MAP in all thegroups. with SCaR and CaR having the highest rise. SR and SCaR had higher sympathetic activity than NR and CaR. Bilateral carotid occlusion test showed decrease baroreflex sensitivity in SR compared with NR while those of SCaR were enhanced without significantly affecting CaR. Also, there was enhanced baroreflex response (BRR) due to renin-angiotensin system inhibition in NR and SR while it was significantly reduced in SCaR but none in CaR. However, there was reduced BRR to parasympathetic inhibition in experimental groups except in CaR. Unmodified sympathetic activity resulted in enhanced BRR in all the groups. The results of the present study suggests that renin-angiotensin and autonomic nervous systems are impaired by dietary salt-loading, while prevention of salt-hypertension by calcium supplement is through modulation of these actions.
Ladipo
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Department of Physiology, College of Medicine, University of Lagos, Idi-Araba, Lagos, Nigeria. chrisladipo@hotmail.com
Egbe
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Ibu
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D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D017704:Baroreflex / Q000187:drug effects*; D001794:Blood Pressure / Q000187:drug effects; D002136:Calcium, Dietary / Q000494:pharmacology*; D002216:Captopril / Q000494:pharmacology*; D006973:Hypertension / Q000139:chemically induced / Q000178:diet therapy / Q000503:physiopathology; D008297:Male; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012084:Renin-Angiotensin System / Q000187:drug effects; D012965:Sodium Chloride / Q000633:toxicity*; D013564:Sympathetic Nervous System / Q000503:physiopathology
D000806:Angiotensin-Converting Enzyme Inhibitors; D002136:Calcium, Dietary; D012965:Sodium Chloride; D002216:Captopril