Why the study?
Does a high-salt diet alter arteriolar nitric oxide activity in normotensive salt-resistant rats?
Does a high-salt diet alter arteriolar nitric oxide activity in normotensive salt-resistant rats?
Answers are grounded in this paper and cite their sources.
High dietary salt intake impairs nitric oxide-mediated vasodilation in specific microvascular beds even in the absence of elevated blood pressure.
This study evaluated the influence of high dietary salt intake on nitric oxide (NO) activity in the arteriolar network of rats resistant to salt-induced hypertension. The spinotrapezius muscle microvasculature was studied in inbred Dahl salt-resistant (SR/Jr) rats fed low (0.45%)- or high (7%)-salt diets for 4-5 wk. Arterial pressures were not different between groups at any time during the study. NO synthesis inhibition with NG-nitro-L-arginine-methyl ester (L-NAME) constricted arcade arterioles in low-salt SR/Jr and dilated arcade arterioles in high-salt SR/Jr. Arcade arteriole dilation to acetylcholine (ACh), but not sodium nitroprusside (SNP), was impaired in high-salt SR/Jr. In contrast, transverse and distal arteriole responses to L-NAME, ACh, and SNP were identical in high- and low-salt SR/Jr. These findings indicate that high salt intake, in the absence of increased arterial pressure, suppresses the influence of basal and evoked NO on vascular tone in arcading arterioles, but not in smaller transverse and distal arterioles. Unaltered SNP responses in high-salt SR/Jr suggest that this effect does not involve a change in arteriolar smooth muscle responsiveness to NO.
No takes yet. Share an insight, caveat, or question.
M. A. Boegehold (1993) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: