1. Baroreflex sensitivity was studied in relation to the development of spontaneous hypertension in rats (SH rats), with normotensive Wistar-Kyoto (WKY) rats as controls. Conscious, freely moving animals were studied at different times, ranging from 4 to 20 weeks after birth. 2. The youngest SH rats (4-6 weeks; n = 10) already had significantly (P less than 0.01) higher mean arterial blood pressure (112 +/- 2 mmHg) than WKY rats of corresponding age (95 +/- 4 mmHg; n = 10). Baroreflex sensitivity did not differ at this age (0.37 +/- 0.04 vs 0.38 +/- 0.05 ms/mmHg). 3. Mean arterial pressure increased rapidly in SH rats during further development, reaching a value of 166 +/- 3 mmHg in 12-20 week old animals (n = 25). In equally old WKY rats blood pressure was significantly (P less than 0.001) lower (110 +/- 6 mmHg, n = 25). Baroreflex sensitivity did not change during development of SH rats (0.40 +/- 0.03 ms/mmHg in 12-20 weeks old SH rats), whereas it increased two- to three-fold in WKY rats (0.93 +/- 0.08 ms/mmHg, P less than 0.001). 4. It is concluded that an increase in baroreflex sensitivity is part of the development of a normotensive cardiovascular system, whereas in SH rats responsiveness of the baroreceptor reflex remains depressed during the development and stabilization of hypertension.

In this study, we investigated the central as well as the regional hemodynamics of spontaneous hypertension in different phases using the reference sample microsphere method in conscious, unrestrained spontaneously hypertensive rats (SHR) using age-matched progenitor Wistar Kyoto rats (WKy) as controls. Moreover, in order to study the role of intravascular fluid volumes and their regional distribution in the early hemodynamics of spontaneous hypertension, we measured albumin distribution spaces at different ages in SHR and WKy. Microsphere studies showed an increase of cardiac output in 5 weeks old SHR when compared to age-matched WKy. This increased flow was mainly transmitted to the muscular and skin vascular bed. The kidney vascular resistance was increased significantly already in 5 weeks old SHR. In 7-8 weeks old animals, cardiac output was not significantly different in SHR and WKy. The increase in blood pressure was then characterized by a generalized increase in vascular resistance in almost all tissues. Plasma volume (PV) measurements indicate a significantly higher PV in 5 weeks old SHR when compared to age-matched WKy. At later ages (7-16 weeks), PV was lower in SHR than in WKy. Regional measurements show a consistently lower PV in gut, muscle, testes, and skin in SHR. It is concluded that the early increase in cardiac output in SHR is related to an increased central intravascular volume, possibly because of renal fluid retention. Moreover, the later further rise in blood pressure and increase in total peripheral resistance seem to be caused by an independent secondary rise in vascular resistance of all vascular beds.

The effect of chronic physical exercise on the development of hypertension was measured in spontaneously hypertensive rats (SHR) and their progenitor normotensive wistar-kyoto controls (WK). Starting 4--5 weeks after birth groups of rats were subjected to swimming exercise 1 h x day-1, 4 days x week-1 for a total period of 11 weeks. Control rats were handled daily without exercise. Both in trained SHR and WK a significant delay in increase in body weight was observed. Physical training caused a small, but significant (P less than 0.001) reduction in systolic blood pressure of SHR, whereas it did not affect blood pressure in WK. Heart rate was significantly (P less than 0.001) lower in both trained SHR and WK than in their non-trained controls. At the end of the training period the degree of training was tested by measuring muscle cytochrome oxidase activity and relative heart weight. Cytochrome oxidase activity in gastrocnemius muscle was higher in the trained animals, although the difference was only significant (P less than 0.05) for WK. Training also caused a significant (P less than 0.01) increase in the ratio heart weight to body weight in WK. Both trained and non-trained SHR have a ca. 25% higher relative heart weight than WK controls. SHR hearts did not further hypertrophy as a consequence of physical exercise. These data indicate that swim training induces a trained state in both SHR and WK. Moreover, this form of training causes a slight, but significant attenuation of the development of hypertension in SHR.

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