Role of angiotensin II, sympathetic stimulation and salt in the development of structural vascular changes in rat kidney.
1. Functional and structural vasoconstriction of renal cortical arteries is the earliest change leading to hypertension. In the present study, the interaction of a subpressor dose of angiotensin (Ang) II, a 2% NaCl diet and sympathetic stimulation in the form of overnight cold exposure was investigated in the development of renal structural vascular changes in male Sprague-Dawley rats. 2. Morphometric measurements of renal cortical resistance arteries and volume density measurements of renal cortical components were performed in eight groups of rats after 12 weeks of treatment: AngII; 2% NaCl diet; cold exposure (5 degrees C); AngII plus 2% NaCl diet; AngII plus cold exposure; cold exposure plus 2% NaCl diet; ANG II plus 2% NaCl diet plus cold exposure; and sham operation and treatment (control). 3. The average weekly systolic blood pressure of AngII-treated plus salt-fed rats was increased, whereas that of cold-stressed plus salt-fed rats at room temperature decreased compared with controls. The blood pressure rise of the former group was accompanied by an increased wall-to-lumen ratio (WLR) of cortical resistance arteries and decreased glomerular volume, whereas the reduction in blood pressure in the latter group was accompanied by a decreased WLR of cortical resistance arteries and increased volume density of cortical renal tubules. There were no changes in either the blood pressure or renal structure of the other groups. 4. There is a parallel relationship between changes in preglomerular structural vascular resistance and changes in blood pressure in rats. It remains to be determined whether renal cortical structural changes are the cause of, or are compensatory for, chronic changes in blood pressure.
Simon
Geza
G
Department of Medicine, VA Medical Center, Minneapolis, Minnesota 55417, USA. simon016@tc.umn.edu
Jäckel
Marta
M
Illyes
Gyorgy
G
D000320:Adrenergic Fibers / Q000187:drug effects / Q000502:physiology*; D000804:Angiotensin II / Q000494:pharmacology / Q000502:physiology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D003080:Cold Temperature / Q000009:adverse effects; D007668:Kidney / Q000098:blood supply / Q000187:drug effects / Q000502:physiology*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012077:Renal Artery / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D017673:Sodium Chloride, Dietary / Q000494:pharmacology*
D017673:Sodium Chloride, Dietary; D000804:Angiotensin II