Chronic blockade of neuronal nitric oxide synthase does not affect long-term control of blood pressure in normal, saline-drinking or deoxycorticosterone-treated rats.
It has been reported that long-term selective inhibition of neuronal nitric oxide synthase (nNOS) produces elevated blood pressure (BP) in normal rats. The present study was designed to analyse the possible influences of the sodium-retaining hormone deoxycorticosterone acetate (DOCA) and of an increased sodium intake on BP effects induced by the chronic blockade of nNOS with 7-nitroindazole (7NI). Two experiments were performed using 7NI at a dose of either 10 mg x kg(-1) x day(-1) (experiment 1) or 30 mg x kg(-1) x day(-1) (experiment 2). The following groups were used in both experiments: control rats, and rats that received either 1 % saline drinking water (Salt), deoxycorticosterone acetate (DOCA), 7NI, 7NI plus 1 % saline (7NI + Salt) or 7NI plus DOCA (7NI + DOCA). The tail systolic BP (SBP) was measured in all rats once a week. At the end of the experimental period, the mean arterial pressure (MAP) and metabolic, morphological and renal variables were measured. There were no significant differences in the tail SBP, final MAP or glomerular filtration rate between the experimental groups and the control group. In both experiments, the plasma renin activity (PRA) was significantly inhibited in the Salt groups and suppressed in the DOCA groups. The PRA significantly increased in the 7NI groups, whereas the 7NI + Salt and 7NI + DOCA groups showed a significant inhibition in PRA, especially compared to the 7NI groups in the two experiments. We conclude that chronic nNOS blockade is unable to increase BP in normal, saline-drinking or DOCA-treated rats. Furthermore, the nNOS blockade does not interfere with the counterbalance between renin and an increased sodium intake or retention.
Wangensteen
Rosemary
R
Departamento de Fisiología, Facultad de Medicina, Servicio de Nefrología, Unidad Experimental, Hospital Virgen de las Nieves, Granada, Spain.
Sainz
Juan
J
Rodríguez-Gomez
Isabel
I
Moreno
Juan Manuel
JM
Osuna
Antonio
A
Vargas
Félix
F
D000803:Angiotensin I / Q000378:metabolism / Q000502:physiology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D003900:Desoxycorticosterone / Q000494:pharmacology*; D005919:Glomerular Filtration Rate / Q000187:drug effects / Q000502:physiology; D007191:Indazoles / Q000494:pharmacology*; D007668:Kidney / Q000187:drug effects / Q000502:physiology; D008297:Male; D009318:Natriuresis / Q000187:drug effects; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D052248:Nitric Oxide Synthase Type I; D011188:Potassium / Q000097:blood; D051381:Rats; D017208:Rats, Wistar; D012083:Renin / Q000097:blood / Q000502:physiology; D012964:Sodium / Q000097:blood; D012965:Sodium Chloride; D012982:Sodium, Dietary
D007191:Indazoles; D012982:Sodium, Dietary; D003900:Desoxycorticosterone; D012965:Sodium Chloride; D000803:Angiotensin I; D012964:Sodium; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I; C496322:Nos1 protein, rat; D012083:Renin; D011188:Potassium; C080122:7-nitroindazole