title: The diastolic decay constant in spontaneously hypertensive rats versus WKY rats as an indicator for vasomotor control.
abstract: This research uses the diastolic decay constant (tau) to investigate the short term mechanism responsible for vasomotor control, mainly the alpha-sympathetic control system. Previous studies have shown that vasomotor control is altered in spontaneously hypertensive rats (SHR) preceding the phase of overt hypertension. The diastolic decay, according to the two element Windkessel model, displays an exponential shape with a decay constant, tau, depending on both the vascular resistance and the compliance. In our experiments, we used tau to characterize vasomotor activity and its control in the normotensive rats as well as in the spontaneously hypertensive rats (SHR) prone to hypertension. The beat to beat value of tau was evaluated from a continuous arterial blood pressure (ABP) signal, measured in the tail artery of the conscious, unrestrained rat. Four months old prehypertensive SHR were compared to their age matched normotensive controls (WKY). To study vasomotor regulation, we computed gains and delay times by investigating the compensatory response in tau to changes in mean ABP (MBP). These parameters are expected in the short term to be neurally controlled by the sympathetic system, mainly alpha-sympathetic. Our set of experiments consisted of changing MBP by performing successive injections in bolus of increasing doses of the vasoconstrictor angiotensin II. This procedure was repeated under double cardiac autonomic blockade of the vagal and beta 1 = sympathetic limbs. Our results show that, under baseline conditions, the absolute gain and delay times of tau are reduced in SHR compared to WKY. Double cardiac blockade decreases the absolute gain in both strains, while abolishing the baseline strain differences. These results reinforce our assumption that, in SHR, the alpha-sympathetic system is in a basic state of excitation even prior to the onset of overt hypertension and therefore reacting with reduced sensitivity (lower gain) to changes in MBP.
authors.affiliation: Physics Department, Tel-Aviv University, Israel.
authors.forename: S
authors.initials: S
authors.lastname: Eyal
authors.forename: O
authors.initials: O
authors.lastname: Oz
authors.forename: S
authors.initials: S
authors.lastname: Eliash
authors.forename: G
authors.initials: G
authors.lastname: Wasserman
authors.forename: S
authors.initials: S
authors.lastname: Akselrod
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001340:Autonomic Nerve Block; D003971:Diastole; D006329:Heart Conduction System / Q000187:drug effects / Q000503:physiopathology; D006973:Hypertension / Q000503:physiopathology*; D009407:Nerve Block; D051381:Rats; D011918:Rats, Inbred SHR / Q000502:physiology*; D011921:Rats, Inbred WKY / Q000502:physiology; D012016:Reference Values; D013997:Time Factors; D014630:Vagus Nerve / Q000503:physiopathology; D014666:Vasomotor System / Q000503:physiopathology*
chemical_list: D000319:Adrenergic beta-Antagonists