The roles of the sympathetic nervous system, angiotensin II, and arginine vasopressin in the cardiovascularrenal responses to nitric oxide synthesis inhibition were examined in eight conscious dogs equipped with arterial and venous catheters and a nonoccluding bladder catheter. Nitric oxide inhibition was achieved by intravenous infusion of TV°-nitro-Larginine methyl ester (L-NAME) at 37.1 nmol/kg per minute for 140 minutes in the control group. The same dogs, after a 1-week recovery, were pretreated for 2 days with either prazosin for a, blockade, prazosin plus propranolol for a, plus /3 blockade, L-158,809 for angiotensin receptor blockade, or d(CH 2 )Tyr(Me)arginine vasopressin for vasopressin-V, blockade, and the L-NAME infusion was repeated. After 140 minutes of L-NAME infusion into the control group, mean arterial pressure and renal vascular resistance had increased 16% and 71%, and renal blood flow, glomerular filtration rate, urine flow, and urinary sodium excretion had decreased 33%, A number of recent studies have shown that nitric oxide (NO) synthesis inhibition causes both L. acute and chronic increases in arterial pressure. 18 In addition, several studies have shown that administration of the NO synthesis inhibitor Af G -nitro-L-arginine methyl ester (L-NAME) causes acute 9 and chronic 12 renal vasoconstriction in rats. Several investigators have also shown that inhibition of NO synthesis enhances the vasoconstrictor actions of a number of neurohumoral systems.1013 Therefore, it is conceivable that some of these pressor and renal vasoconstrictor effects of NO synthesis inhibition could be mediated by other neurohumoral factors.NO synthesis inhibition in anesthetized rats has been shown to cause at least a short-term increase in renal nerve activity.10 Also, application of L-NAME to isolated afferent arterioles amplified the acute vasoconstrictor effects of angiotensin II (Ang II).11 In addition, acute NO synthesis inhibition amplified the pressor effects of arginine vasopressin (AVP).12 -13 Therefore, NO release may oppose the effects of several vasoconstrictor systems.A recent study in anesthetized rats showed that the pressor and renal vasoconstrictor effects of L-NAME were not attenuated during individual or combined blockade of all the major vasoconstrictor systems.5 However, another study in anesthetized rats showed that 16%, 61%, and 64%, respectively. The decrement in renal blood flow and glomerular filtration during L-NAME administration was unaffected by any of the neurohumoral blockers. During V, blockade L-NAME resulted in only a 3% increase in arterial pressure, attenuation of the renal vascular resistance response, and almost total elimination of the decrease in urine flow. During angiotensin blockade the L-NAME-induced increase in arterial pressure was markedly attenuated, and the decrease in urinary sodium excretion was attenuated in the a, plus f3 blockade group. In conclusion, short-term renal and cardiovascular effects of nitric oxide synthesis inhibition in conscious dogs...

This paper describes a fully automatic oil-pipe-line pumping station built by the A.S.M.E. Special Research Committee on Automatic Pipe-Line Pumping Stations. The station is in operation at the grounds of the International Petroleum Exposition at Tulsa, Okla., and is being used as an experimental laboratory to complete the development of automatic pumping and to fully test out and coordinate the equipment units used in its construction. When this development is completed, the committee will make a final report indicating all changes, and will give a description of the piping and electrical circuits finally resulting from this research.