title: Effect of haemorrhage on the power of low frequency blood pressure fluctuations in young spontaneously hypertensive rats.
abstract: 1. Before the onset of hypertension low frequency (0.04-0.1 Hz) MAP fluctuations are reduced in SHR when compared to WKY. We studied the effect of haemorrhage under alpha1 blockade or angiotensin converting enzyme inhibition (CEI) on the power spectra (PS) of each strain. 2. MAP was recorded from the caudal artery in conscious, 1 month old SHR and WKY. Three groups of rats were studied. Group 1, acute 2 mL haemorrhage; groups 2 and 3, injection of prazosin (0.25-2.5 mg/kg) or captopril (0.5-4 mg/kg), followed by haemorrhage, as in group 1. The PS was divided into 3 frequency bands, 0.004-0.04, 0.04-0.07 and 0.07-0.1 Hz. 3. In SHR, although the baseline MAP levels were similar to those of WKY, the PS was significantly damped in each of the 3 frequency bands. 4. Haemorrhage induced a similar MAP fall in both strains accompanied by an increase in the slow MAP fluctuations. However, in SHR the PS response was significantly greater than in WKY. The biggest response was in the slowest (0.004-0.04 Hz) frequency band, 8.7 +/- 1.7 vs 1.5 +/- 0.4 times baseline levels, respectively. 5. The difference between the two strains in the PS response to haemorrhage was eliminated by alpha1 blockade. The exaggerated response observed in haemorrhaged, unblocked SHR was reduced in the 3 frequency bands. 6. Captopril reduced the PS response to haemorrhage in SHR to the level observed in WKY in all 3 frequency bands. 7. The enhanced amplification of the MAP fluctuations in haemorrhaged SHR may indicate that SHR requires greater recruitment of control mechanisms than WKY to maintain MAP at a similar level to WKY.
authors.affiliation: Sackler School of Medicine, Department of Physiology and Pharmacology, Tel Aviv University, Ramat Aviv, Israel.
authors.forename: S
authors.initials: S
authors.lastname: Eliash
authors.forename: O
authors.initials: O
authors.lastname: Oz
authors.forename: S
authors.initials: S
authors.lastname: Akselrod
authors.forename: S
authors.initials: S
authors.lastname: Cohen
mesh_terms: D058646:Adrenergic alpha-1 Receptor Agonists; D058668:Adrenergic alpha-1 Receptor Antagonists; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D002216:Captopril / Q000494:pharmacology; D006470:Hemorrhage / Q000503:physiopathology*; D006973:Hypertension / Q000235:genetics / Q000503:physiopathology*; D011224:Prazosin / Q000494:pharmacology; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY
chemical_list: D058646:Adrenergic alpha-1 Receptor Agonists; D058668:Adrenergic alpha-1 Receptor Antagonists; D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D002216:Captopril; D011224:Prazosin