ABSTRACT
INTRODUCTION: The mechanisms responsible for genesis of salt-induced hypertension and its prevention by dietary calcium supplementation are still not clear. Hence, the effect of salt (NaCl) and calcium supplement on blood pressure and renal excretion were investigated. METHODOLOGY: Daily food consumption, water, salt and calcium intake, as well as urine volume and pH were determined. At the end of the feeding period, animals were anaesthetised and the electrocardiographic and blood pressure measurements were done. RESULTS: Salt-loaded rats (SR) consumed more salt and water but less calcium, and excreted more urine and hydrogen ion than control rats (NR). There was elevation of mean arterial pressure (MAP) in SR (132.63 +/- 2.3 mmHg) compared with NR (94.00 +/- 2.2 mmHg) but there was no significant difference in their heart rates (HR) (395 +/- 11.7 vs. 429 +/- 15.4 beats/min). However, salt-loaded-calcium-fed rats (SCaR) had similar MAP as NR (99.29 +/- 1.8 mmHg) and a lower HR (379 +/- 14.9 beats/min). A reduction in water consumption and an increase in urine output as well as urinary hydrogen ion were noted in SCaR compared with SR. Calcium alone (CaR) did not have any effect on MAP (88.01 +/- 1.3 mmHg) and HR (413 +/- 7.98 beats/min). There was no difference in the organ/body-weight ratios of the aortae among the experimental rats. However, there was renal hypertrophy in SR and SCaR. Also, the hearts of SR were bigger than CaR. The mean electrical axis of hearts showed a tendency towards left ventricular hypertrophy in SR, which was greater than SCaR. CONCLUSION: The results suggest that salt loading caused renal hypertrophy and a tendency towards left ventricular hypertrophy. There are associated salt and water retention resulting in alteration of some cardiovascular function. Dietary calcium supplementation reversed these functional defects.
Subject(s)
Blood Pressure/drug effects , Calcium, Dietary/pharmacology , Kidney/drug effects , Sodium, Dietary/pharmacology , Animals , Blood , Blood Pressure/physiology , Calcium, Dietary/administration & dosage , Electrocardiography , Heart Rate/drug effects , Heart Rate/physiology , Hypertrophy , Hypertrophy, Left Ventricular/physiopathology , Kidney/pathology , Kidney/physiology , Male , Models, Animal , Organ Size/drug effects , Rats , Rats, Sprague-Dawley , Sodium, Dietary/administration & dosage , UrineABSTRACT
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.
