1. Cardiovascular reactivity, blood vessel morphology, blood pressure and the activity of the renin—angiotensin system were determined in the 3-week-old spontaneously hypertensive (SHR), Wistar—Kyoto (WKY) and outbred Wistar (WIS) rat.
2. In an isolated perfused mesenteric artery preparation the SHR had a significantly increased maximum response to KCl and noradrenaline (P < 0.02) compared with the WKY. Using a myograph, vascular structure was measured over a range of resistance arteries and showed a significant correlation between lumen diameter and both media cross-sectional area and thickness, with the regression line for the SHR shifted upwards indicating both increased media area and thickness. This was associated with a slight, but significant, narrowing of the lumen (P < 0.01) and an increased media/lumen ratio (0.049 ±0.01, 0.034 ±0.007, 0.036 ±0.008 for SHR, WKY and WIS, respectively, means ±sd P < 0.001). The SHR had a greater heart/body weight ratio than either the WKY or the WIS (P < 0.001).
3. Both mesenteric artery and membrane protein content were higher in the SHR, indicating an increase in cell size or number.
4. Plasma renin activity (means ±sd) was lower in the SHR (1.0 ± 0.7 pmol of angiotensin I h−1 ml−1) than in the WKY (2.2±1.2 pmol of angiotensin I h−1 ml−1, P < 0.001) but not different from that in the WIS (1.2±0.8 pmol of angiotensin I h−1 ml−1). Mesenteric artery vascular renin concentration was also lower in the SHR (P = 0.06). Plasma angiotensin II concentration (mean±sd) was similarly lower in the SHR (11.9 ±3.8 fmol/ml) than in the WKY (18.8 ± 6.2 fmol/ml, P < 0.001) but not different from that in the WIS (14.5 ±5.8 fmol/ml). There was no difference in angiotensin II receptor number or affinity between the three rat strains.
5. Quiescent intra-arterial blood pressure was significantly higher in the SHR both 1 and 2 days after cannula insertion. On day 2 the pressure (mean ± sd) in the SHR was 112.7 ± 19.9 mmHg, in the WKY 81.1 ± 14.4 mmHg and in the WIS 75.1 ± 7.8 mmHg (P < 0.001).
6. These data indicate the presence of marked vascular and cardiac hypertrophy in the SHR at a very early period in its development. Blood pressure is elevated and there is no overactivity of the renin system. We conclude that, at this time, there is no prehypertensive phase nor is there evidence of angiotensin II-mediated pressure-independent mechanism in the hypertrophic development.
