Why the study?
Does high salt intake and angiotensin II infusion alter microvessel density in normal rats?
Does high salt intake and angiotensin II infusion alter microvessel density in normal rats?
High salt intake reduces microvessel density in rats, which can be prevented by maintaining normal plasma angiotensin II levels, suggesting the rarefaction is driven by a dietary-induced fall in angiotensin II.
Animal data on salt-induced rarefaction do not inform human sodium guidance; leaves open angiotensin II mediation in clinical microvascular disease.
This study investigated the effect of salt intake and angiotensin II (ANG II) levels on microvessel density (MVD). Rats with indwelling arterial and venous catheters were placed on either a high-salt (HS; 4%) or a low-salt diet (LS; 0.4%) for 2 or 4 wk, and blood pressure, heart rate, and plasma renin activity were measured. Plasma ANG II was fixed at normal levels in half of the rats on HS by continuous intravenous infusion of ANG II (5 ng.kg-1.min-1). Samples of cremaster muscle were examined histologically to determine MVD. No difference in MVD was observed between HS and LS groups after 2 wk. After 4 wk on HS, MVD was reduced (22.4%, P less than 0.05) compared with the LS group. In rats fed HS, ANG II infusion induced a significant dose-dependent increase in MVD from 85.11 +/- 3.34 to 98.94 +/- 4.62 (ANG II, 5 ng.kg-1.min-1) and to 107.60 +/- 7.00 (ANG II, 10 ng.kg-1.min-1) (P less than 0.05), with no change in blood pressure. Maintenance of ANG II levels for 4 wk blocked the rarefaction due to salt. These results suggest that the decrease in MVD due to salt could be the result of a dietary-induced fall in plasma ANG II levels.
No takes yet. Share an insight, caveat, or question.
Hernández et al. (1992) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: