Hemodynamic, Morphometric and Autonomic Patterns in Hypertensive Rats - Renin-Angiotensin System Modulation

Abstract

BACKGROUND:Spontaneously hypertensive rats develop left ventricular hypertrophy, increased blood pressure and blood pressure variability, which are important determinants of heart damage, like the activation of renin-angiotensin system.AIMS:To investigate the effects of the time-course of hypertension over 1) hemodynamic and autonomic patterns (blood pressure; blood pressure variability; heart rate); 2) left ventricular hypertrophy; and 3) local and systemic Renin-angiotensin system of the spontaneously hypertensive rats.METHODS:Male spontaneously hypertensive rats were randomized into two groups: young (n=13) and adult (n=12). Hemodynamic signals (blood pressure, heart rate), blood pressure variability (BPV) and spectral analysis of the autonomic components of blood pressure were analyzed. LEFT ventricular hypertrophy was measured by the ratio of LV mass to body weight (mg/g), by myocyte diameter (μm) and by relative fibrosis area (RFA, %). ACE and ACE2 activities were measured by fluorometry (UF/min), and plasma renin activity (PRA) was assessed by a radioimmunoassay (ng/mL/h). Cardiac gene expressions of Agt, Ace and Ace2 were quantified by RT-PCR (AU).RESULTS:The time-course of hypertension in spontaneously hypertensive rats increased BPV and reduced the alpha index in adult spontaneously hypertensive rats. Adult rats showed increases in left ventricular hypertrophy and in RFA. Compared to young spontaneously hypertensive rats, adult spontaneously hypertensive rats had lower cardiac ACE and ACE2 activities, and high levels of PRA. No change was observed in gene expression of Renin-angiotensin system components.CONCLUSIONS:The observed autonomic dysfunction and modulation of Renin-angiotensin system activity are contributing factors to end-organ damage in hypertension and could be interacting. Our findings suggest that the management of hypertensive disease must start before blood pressure reaches the highest stable levels and the consequent established end-organ damage is reached.

Eccentric and concentric cardiac hypertrophy induced by exercise training: microRNAs and molecular determinants

“…An increase of 480/350 (systolic and diastolic) BP has been shown in bodybuilders while performing leg press exercise (6,7). Concentric cardiac hypertrophy might also result from pressure overload observed in many pathologic conditions, such as hypertension (8). However, this type of hypertrophy is followed by diastolic and/or systolic dysfunction and a disproportionate increase in the thickness of the left ventricle posterior wall and interventricular septum (8)(9)(10).…”

“…Concentric cardiac hypertrophy might also result from pressure overload observed in many pathologic conditions, such as hypertension (8). However, this type of hypertrophy is followed by diastolic and/or systolic dysfunction and a disproportionate increase in the thickness of the left ventricle posterior wall and interventricular septum (8)(9)(10). Sometimes, the physiological hypertrophy developed by high level strength athletes presents a macroscopic structure similar to pathological hypertrophy, which could be incorrectly interpreted as pathological.…”

Effect of Tulbaghia violacea on the blood pressure and heart rate in male spontaneously hypertensive Wistar rats

“…In vivo studies have shown that the SHR has an increased cardiac output (CO) with normal total peripheral resistance (TPR) in the early stages of HTN, but as the animal progresses into the established HTN state, the CO returns to normal while the hypertrophied blood vessels produce an increase in the TPR (Smith & Hutchins, 1979). The SHR also develops left ventricular hypertrophy (LVH), increased BP and BP variability; all of which are important indices of heart damage (Zamo et al, 2010). An advantage of the SHR is that compounds which lower BP in this strain also lower BP in hypertensive humans.…”

“…The RAABS/RAAS is a key physiologic regulator of vascular tone, salt and water balance, BP, bradykinin system and pituitary gland hormones (Gradman, 2009;Lacolley et al, 2009;Zamo et al, 2010). Short term activation of the system is geared towards maintaining intravascular volume, BP, and tissue repair; however, chronic activation leads to chronic vasoconstriction and elevation of BP, VSMC growth/migration, endothelial dysfunction, oxidative stress, the release of cytokines and inflammatory cell activation, fibrosis, and thrombosis.…”

The renin–angiotensin system is modulated by swimming training depending on the age of spontaneously hypertensive rats

“…Previously, we investigated the RAS modulation during the timecourse of hypertension, and the effects on hemodynamic and morphometric parameters (Zamo et al 2010). This work was undertaken to investigate the effects of swimming training (ST) in different stages of hypertension on 1) hemodynamic patterns (blood pressure and heart rate); 2) left ventricular hypertrophy and collagen volume fraction; and 3) local and systemic RAS of spontaneously hypertensive rat (SHR).…”