Nitric Oxide Modulation of Neurally Induced Proximal Tubular Fluid Reabsorption in the Rat

• Published in: Hypertension (Dallas, Tex. 1979) Vol. 39; no. 3; pp. 790 - 793
• Main Authors: Wu, Xiao Chun, Johns, Edward J
• Format: Journal Article
• Language: English
• Published: Philadelphia, PA American Heart Association, Inc 01.03.2002; Hagerstown, MD Lippincott
• Subjects: Absorption - drug effects; Animals; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Blood and lymphatic vessels; Blood Pressure - physiology; Body Fluids - metabolism; Cardiology. Vascular system; Electric Stimulation; Enzyme Inhibitors - pharmacology; Experimental diseases; Glomerular Filtration Rate; Guanidines - pharmacology; Indazoles - pharmacology; Kidney Tubules, Proximal - drug effects; Kidney Tubules, Proximal - innervation; Kidney Tubules, Proximal - metabolism; Male; Medical sciences; NG-Nitroarginine Methyl Ester - pharmacology; Nitric Oxide - metabolism; Nitric Oxide Donors - pharmacology; Nitric Oxide Synthase - antagonists & inhibitors; Nitroprusside - pharmacology; Rats; Rats, Wistar; Sodium - urine; Sympathetic Nervous System - physiology; Urination; Hypertension; Rat; Pathogenesis; Rodentia; Cardiovascular disease; Sympathetic nervous system; Kidney; Vertebrata; Mammalia; Sodium; Animal; Nitric oxide; Tubular reabsorption; Proximal tube
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/hy0302.105681

This study investigated the role of NO in mediating the renal sympathetic nerve–mediated increases in proximal tubular fluid reabsorption (Jva). In inactin-anesthetized Wistar rats, renal sympathetic nerve stimulation (15 V, 2 ms) at 0.75 and 1.0 Hz did not change blood pressure or glomerular filtration rate but did decrease urine flow and sodium excretion in a frequency-related fashion by 40% to 50% at 1.0 Hz (both, P <0.01). Renal nerve stimulation in control animals increased Jva by 11% at 0.75 Hz (P <0.05) and 31% at 1.0 Hz (P <0.01). Intraluminal Nω-nitro-l-arginine methyl ester (L-NAME) resulted in a higher basal Jva (19%, P <0.05), and renal nerve stimulation had no effect on Jva. When L-NAME plus sodium nitroprusside was present intraluminally, however, there were frequency-dependent increases in Jva that were similar in pattern and magnitude to the control rats. Introduction of the relatively selective nNOS blocker 7-nitroindazole intraluminally, at 10 and 10 M, raised basal Jva by 18% and 24%, respectively (P <0.01), and renal nerve stimulation did not change Jva. Intraluminal aminoguanidine (10 M), a relatively selective iNOS blocker, did not affect basal Jva, which remained unchanged during renal nerve stimulation. These data are consistent with NO exerting a tonic inhibitory action on the basal levels of Jva, which, in part, is caused by NO generated by the nNOS isoform. Moreover, the findings have revealed that the presence of NO is necessary to ensure that renal nerves can stimulate fluid reabsorption by the proximal tubules, requiring NO generated from both nNOS and iNOS.