Insight into blood-pressure control in SHR via the response to acute hemorrhage: a spectral analysis approach.
In this study we investigated, by means of the spectral analysis approach, the possible alterations in the activity of the pressor-control mechanisms in relation to the development of essential hypertension. Since the maintenance of controlled arterial blood pressure (ABP) levels is achieved by a continuously fluctuating control system, instantaneous ABP varies continuously in direct correlation with the activation of various control branches. The power spectrum of ABP fluctuations thus provides a quantitative measure of the activity of the various controlling mechanisms. Two strains of rats, Spontaneously Hypertensive Rats (SHR) and Wistar-Kyoto normotensive rats (WKY), were subjected to acute hemorrhage, a procedure known to trigger a strong response, of both the neural (autonomic nervous system) and the hormonal (renin-angiotensin and vasopressin) systems. ABP was continuously recorded from the caudal artery in conscious, 1-month-old SHR and WKY. Three groups of rats were studied. Group 1, acute 2-ml hemorrhage; Groups 2, injection of prazosin (2.5 mg/kg) or Group 3, captopril (4 mg/kg), each followed by bleeding as in the group 1. Spectral analysis of ABP fluctuations was performed on time traces of 20 min duration. The low-frequency part of the power spectrum was analyzed. Three frequency bands were investigated: 0.004-0.04 Hz, 0.04-0.07 Hz and 0.07-0.1 Hz. In SHR, although the baseline mean ABP levels were similar to those of WKY, ABP fluctuations were significantly dampened in SHR in each of the three frequency ranges. Hemorrhage induced, in both strains, a similar fall in mean ABP accompanied by an increase in the slow ABP fluctuations. However, in SHR, the response was significantly greater that that of WKY. The steepest response was observed in the slowest, 0.004-0.04 Hz frequency band, 8.7 +/- 1.7 vs. 1.5 +/- 0.4 times the baseline levels. However, this intense increase in power after hemorrhage brought the two strains to similar levels. The difference in the response to bleeding was eliminated, in the three frequency ranges, by alpha 1 blockade. Captopril reduced the response to bleeding in SHR, to the level observed in WKY in all three frequency bands. Spectral analysis of the spontaneous oscillations in ABP unmasks abnormalities which conventional blood pressure measurements cannot detect in 1-month-old, still normotensive SHR. It thus, provides a tool to study the dynamics of the abnormalities which precede the development of hypertension. Bleeding amplifies the malfunction observed in SHR under baseline conditions, since the mean ABP levels were similar in both strains before and after bleeding, SHR seem to retain the ability to respond to a fall in blood volume by requiring a greater recruitment of the control mechanisms than WKY.
Oz
O
O
Physics Department, Tel-Aviv University, Israel.
Eliash
S
S
Cohen
S
S
Akselrod
S
S
D000208:Acute Disease; D058668:Adrenergic alpha-1 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D001794:Blood Pressure / Q000502:physiology*; D002216:Captopril / Q000494:pharmacology; D006470:Hemorrhage / Q000503:physiopathology*; D006973:Hypertension / Q000235:genetics / Q000503:physiopathology*; D008297:Male; D011224:Prazosin / Q000494:pharmacology; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D012084:Renin-Angiotensin System / Q000187:drug effects
D058668:Adrenergic alpha-1 Receptor Antagonists; D000317:Adrenergic alpha-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D002216:Captopril; D011224:Prazosin