STRUCTURAL AND FUNCTIONAL RESISTANCE VESSEL ABNORMALITIES IN THE SPONTANEOUSLY HYPERTENSIVE RAT AS REVEALED BY IN VIVO VASODILATOR INTERVENTION (CALCIUM BLOCKERS)

• Main Author: REED, BRIAN VAUGHN
• Format: Dissertation
• Language: English
• Published: ProQuest Dissertations & Theses 01-01-1985
• Subjects: Anatomy & physiology; Animals; Physiology
• ISBN: 9798205575256

The purpose of the study was to determine the differences in regional vascular resistances and blood flows between spontane- ously hypertensive rats (SHR) and normotensive Wistar Kyoto (WKY) rats, and to the extent possible, to characterize various SHR vascular beds as having structural and/or functional alterations. The sample consisted of 28 SHRs (MAP* 178.8 (+OR-) 16.8 mm Hg) and 24 WKYs (MAP* 112.9 (+OR-) 18.1 mm Hg; p < 0.001), all of which were males between 18 and 20 weeks of age. When normalized with respect to body weight, systemic hemodynamics were as expected: cardiac index was similar for SHRs and WKYS while total peripheral resistance index (TPRI) was significantly higher for SHRs. The hemodynamic variables were measured in control SHRs and WKYs as well as in animals which received low (30 (mu)g/kg) or high (100 (mu)g/kg) nifedipine, a vascular smooth muscle relaxant. Meas- urements were made by means of an isotope-labeled microsphere technique under pentobarbital anesthesia (50 mg/kg i.p.). Nine vasculatures were sampled: renal, bronchial, coronary, stomach, brain, skeletal muscle, duodenum, spleen, and liver. While SHR regional resistances were found to be elevated in all of the vascular beds, significantly reduced blood flows indicated that resistance was most elevated in the SHR kidney, stomach, and spleen. Because nifedipine did not have a strain-specific effect on TPRI, the data suggested that on the whole, structural alterations of SHR vasculatures contributed more to the elevated TPR of the SHR than functional alterations did. A SHR-specific effect of nifedipine suggested functional altera- tions in several vasculatures, most notably the kidney, and to a lesser degree, the bronchial, coronary, and stomach vasculatures. The simultaneous existence of structural alterations at those vasculatures was suggested by the inability of nifedipine to equalize SHR and WKY resistances, even at the high dose level. There was evidence of only structural alterations in the SHR skeletal muscle samples since high dose nifedipine had a strain-specific effect on WKY resistances and flows at that organ. The study was unable to discriminate structural from functional vascular alterations in the remaining sampled organs. *Mean Arterial Pressure