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Contribution of Extrinsic Factors and Intrinsic Vascular Alterations to Reduced Arteriolar Reactivity with High‐Salt Diet and Hypertension
Author(s) -
FRISBEE JEFFERSON C.,
SYLVESTER FRANCIS A.,
LOMBARD JULIAN H.
Publication year - 2000
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1111/j.1549-8719.2000.tb00128.x
Subject(s) - endocrinology , medicine , dilator , sodium nitroprusside , vasodilation , chemistry , skeletal muscle , arteriole , microcirculation , cremaster muscle , nitric oxide , biology
Objective : To determine whether the impaired relaxation of skeletal muscle arterioles of rats on high‐salt diet or with reduced renal mass hypertension (RRM‐HT) represents intrinsic alterations to microvessels alone, or whether extravascular influences also contribute to reduced dilator responses. Methods : Normotensive (NT) Sprague‐Dawley rats were fed low‐salt (LS) or high‐salt (HS) diets, and RRM‐HT rats were fed HS diet for 4–6 weeks. In situ and isolated cremaster muscle first‐order arterioles (1A) were examined using television microscopy, and a video micrometer was used to measure diameter changes in response to acetylcholine (ACH), cholera toxin (CT), and sodium nitroprusside (SNP). Results : Compared to normotensive low‐salt (NT‐LS) rats, responses of 1A to the agonists were reduced in normotensive high‐salt (NT‐HS) and RRM‐HT rats. Arteriolar reactivity to the agonists in NT‐LS rats and in NT‐HS rats was not different between in situ and in vitro environments. However, in RRM‐HT rats, the reactivity of 1A to each agonist was greater in isolated arterioles than in in situ arterioles. Conclusions : These results suggest that the impaired response of skeletal muscle arterioles to vasodilator stimuli in normotensive rats on high‐salt diet primarily reflects alterations to microvessels alone, while reduced dilator responses in RRM‐HT rats represent a combination of extravascular influences and intrinsic alterations to arterioles themselves.