The small arteries play an important functional role in establishing the increased peripheral resistance found in essential hypertension. This paper concerns the direct measurement of the intrinsic mechanical and contractile properites of two categories of small arterial resistance vessels in the mesenteric bed of 5-month-old normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). The vessels had mean internal diameters of 246 fim and 153/* m when relaxed at 100 mm Hg effective transmural pressure. Segments (1 mm) were mounted in such a way that internal circumference could be controlled and the circumferential wall tension (T) measured. After mounting, each vessel was maximally activated (by K* depolarization at 37 C in the presence of 5 mM Ca2+) at an internal circumference for which AT was approximately maximal, where AT= Tactlve-Trelaxed. From the average values of AT measured we have estimated (on the basis of Laplace's equation) that the SHR vessel would average values of AT measured we have estimated (on the basis of Laplace's equation) that the SHR vessels would have been able to contract against 34% greater pressures than the WKY vessels (P< 0.001). Optical measurements of the dimensions of these vessels showed a 23% greater wall thickness in the SHR vessels (P< 0.02). There were no significant differences in the calculated active wall stresses of the SHR and WKY vessels; this suggests that the greater contractility found in the SHR vessels may be due to their having a greater smooth muscle cell content. These vessel measurements have been examined as well as the rats' blood pressures and heart to body weight ratios. The comparison points to the possibility that the disturbance to the cardiovascular regulatory system which results in hypertension produces similar cellular responses in both the myocardium and the peripheral vasculature.

HUMAN essential hypertension is associated with an elevated blood pressure but a normal cardiac output. 1 The total peripheral resistance is therefore elevated. The cause of this elevation is not clear but a genetic factor seems to be involved. 2-3 As a means to investigate genetic hypertension in detail, a strain of spontaneously hypertensive rats (SHR) has been developed by Okamoto and his colleagues4 from a colony of Wistar-Kyoto rats (WKY). These SHR reach a stage of established hypertension by the age of 5 months. At this time their systolic blood pressure is about 50% higher than that of their WKY controls although, as in human essential hypertension, their cardiac output is normal. 5 The vascular bed of these rats contains vessels with diameters ranging from 3 mm in the aorta to about 7^ m in the capillaries. Although all these vessels must contribute to the resistance of the vascular bed to some extent, it is in general the smaller arterial resistance vessels which present the greatest resistance, and which are most involved in regulating blood flow and capillary pressure. 6 Perfusion studies on isolated vascular beds7"" have provided valuable insight into their general mode of action. Such studies are not, however, able to analyze the specific contribution of the various parts of the vascular bed.