Renomedullary interstitial cell lipid droplet content is increased in spontaneously hypertensive rats and by low salt diet

Objective To compare the volumes of renomedullary interstitial cell (RMIC) lipid droplets (putative source of vasodepressor substance) in spontaneousl y hypertensive (SHR) and Wistar-Kyoto (WKY) rats on high and low salt diets as an indication of whether the renomedullary vasodepressor system of the SHR is defective. Methods Ten-week-old male SHR and WKY rats received a low (0.05% w/w) or hi gh salt (5.0%) diet for 21 days. Conscious mean arterial pressure (MAP) was measured and the renal papilla perfusion fixed with a high osmolarity fixa tive. Using electron microscopic stereological techniques, the volume densi ty of lipid in RMIC (V-VLipid,RMIC) and the total volumes of lipid (V-Lipid ) and RMIC (V-RMIC) in papilla were measured. Results MAP of SHR (high 155 +/- 3 mmHg; low 151 +/- 3 mmHg) was significan tly greater than WKY rats (high 126 +/- 2 mmHg; low 129 +/- 2 mmHg; P < 0.0 01), however salt diet had no significant effect on MAP. The VLipid Of rats On the low salt diet was approximately 2.5 times greater than in rats on t he high salt diet (P < 0.01), SHR had significantly greater VLipid than WKY rats irrespective of salt diet (P < 0.05; SHR-low 0.245 +/- 0.031 mm(3), S HR-high 0.093 +/- 0.007 mm(3); WKY-low 0.126 +/- 0.032 mm(3), WKY-high 0.05 1 +/- 0.020 mm(3)). Similar differences were seen for V-VLipid,V-RMIC, howe ver VRMIC was not different between rat strains or salt diet groups. Conclusions SHR and WKY rats responded similarly to the altered salt diets, and SHR demonstrated greater volumes of stored RMIC lipid droplets irrespe ctive of the level of salt intake. These results indicate that SHR hyperten sion is not due to a deficiency in the amount of lipid droplets, the putati ve source of the renomedullary vasodepressor substance and that the renomed ullary vasodepressor system of the SHR is capable of responding normally to the physiological stimulus of altered salt intake. I Hypertens 19:1309-131 3 (C) 2001 Lippincott Williams & Wilkins.