Session I. NITRIC OXIDE IN SALT HYPER- TENSION THE BALANCE OF NITRIC OXIDE AND PRESSOR SYSTEMS IN VARIOUS FORMS OF EXPERIMENTAL HYPERTENSION IN THE RAT

The balance between the principal depressor system (nitric oxide NO) and main pressor systems (renin-angiotensin system RAS, sympathetic nervous system SNS) was studied in two different models of experimental hypertension salt hypertensive Dahl rats and rats made hypertensive by chronic NO synthase inhibition by L-NAME. The animals were subjected to consecutive acute blockade of RAS (captopril 10 mg/kg i.v.) and SNS (pentolinium 5 mg/kg) which was followed by acute bolus of L-NAME (30 mg/kg) and aminoguanidine (inducible NOS inhibitor, AMG 50 mg/kg). Both forms of hypertension are characterized by augmented pentolinium-induced BP fall compared to the respective controls, whereas depressor response to acute captopril injection was slightly increased in L-NAME hypertensive rats only. On the other hand, BP elevation after acute L-NAME injection was not significantly enhanced in salt hypertensive Dahl rats. The same was true for L-NAME hypertensive rats, if their NO synthase was acutely inhibited by AMG. Although total BP rise induced by L-NAME plus AMG administration was comparable in normotensive and hypertensive rats, there was a relative deficit of depressor systems to compensate the augmented activity of pressor systems. It is evident that both apparently contrasting hypertensive models are characterized by 1) the enhanced contribution of SNS to BP maintenance, and 2) the relative NO deficiency facing the enhanced activity of pressor systems (RAS and SNS). Partially supported by GACR 305/03/0769, 305/02/P066, VEGA 2/3185/23, AVOZ 5011922, APVT 51-017902.