Aortic smooth muscle cells from spontaneously hypertensive rats (SHR) exhibit inappropriate proliferation characteristics in culture that suggest a modified response to serum mitogens or growth factors. The present study compares vascular smooth muscle cells from SHR and normotensive Wistar-Kyoto (WKY) rats with respect to their proiiferative and functional response to growth factors. Specific attention was focused on the interaction of these vascular smooth muscle cells with epidermal growth factor. An increased growth rate of vascular smooth muscle cells from SHR (vs. WKY rats) was observed when cells were cultured in the presence of serum (10% and 0.5%), but not under serum-free conditions. The additional presence of low serum concentrations (0.5%) was required for epidermal growth factor to elicit a proiiferative response, whereupon smooth muscle cells from SHR displayed an increased (vs. WKY rats) growth rate. Saturation binding of [ u5 I]epidermal growth factor to intact smooth muscle cells indicated a twofold increase in receptor density in SHR-derived cells (p<0.001 vs. WKY rats) without an alteration in affinity for the growth factor. Cells derived from SHR also exhibited greater functional responsiveness to epidermal growth factor when compared with smooth muscle cells from WKY rats as evidenced by amplifications of both S 6 kinase activation, phosphoinositide catabolism, elevation of intracellular pH, and DNA synthesis (nuclear labeling). We conclude that increased responsiveness of SHR-derived smooth muscle cells to epidermal growth factor could contribute to alterations in vascular smooth muscle growth and tone that may be fundamental to the pathogenesis of hypertension and atherosclerosis. {Hypertension 1989;13:295-304)

A comparison of salivary flow rates was made between three groups of female individuals according to their menopausal status. The three groups consisted of healthy, dentate, nonmedicated women (with the exception of the use of estrogen) from the Baltimore Longitudinal Study of Aging. One group consisted of premenopausal women (n = 51), their mean age was 39 years. Another group (n = 26) was perimenopausal with a mean age of 48 years. A third group (n = 76) was postmenopausal with a mean age of 69 years. The groups were evaluated for unstimulated (U_PAR) and stimulated parotid gland flow rates (S_PAR), unstimulated (U_SUB) and stimulated submandibular/sublingual gland flow rates (S_SUB), and stimulated whole-saliva flow rates (S_WHOLE). The parotid flow rates were determined using a Carlson-Crittenden cup, while the submandibular/sublingual flow rates were determined using the National Institute of Dental Research collector. A 2% citrate solution was used for stimulation in glandular collections. Chewing a 1-cm³ cube of paraffin was used to stimulate whole saliva. The results showed no significant differences in U_PAR, S_PAR, and S_WHOLE between the three groups. However, the premenopausal women had higher U_SUB than the postmenopausal group. The premenopausal women also had higher S_SUB than perimenopausal and postmenopausal groups. There were no differences in salivary flow rates between those taking estrogen and those that were not medicated.

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Smooth muscle cell proliferation is regulated through the coordinated action of growth inhibitors and growth factors/mitogens; a specific heparin-epidermal growth factor (EGF) complementation has been proposed (Reilly et al., 1987, J. Cell. Physiol., 131:149-157). In culture, vascular smooth muscle cells (VSMC) from spontaneously hypertensive rats (SHR) proliferate more rapidly than VSMC from control Wistar Kyoto rats (WKY). We observed that, compared with WKY-derived VSMC, cells from SHR were markedly less susceptible to growth inhibition both by heparin and its homopolysaccharide analogue pentosan polysulphate (PPS). SHR-derived VSMC exhibited a reduced capacity for binding of [3H]heparin to specific extracellular surface receptors, whereas affinities for heparin were comparable between both VSMC isolates. The early (0-2 hr at 37 degrees C) kinetics of internalization did not differ between SHR- and WKY-derived VSMC, but both internalized equivalent proportions (approximately 10%) of initially surface-bound heparin. VSMC from SHR exhibited a greater capacity, without a changed affinity, for [I125]EGF binding than VSMC from WKY. Pre-exposure of VSMC to heparin or PPS decreased, in a time-dependent manner, the EGF binding capacity for both SHR and WKY (by 40-50% after 72 hr). However, in absolute terms, the EGF-binding capacity of VSMC from SHR exposed to heparinoids was similar to that of nonexposed VSMC from WKY.

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