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Background of Increased Flow Resistance and Vascular Reactivity in Spontaneously Hypertensive Rats
325
Citations
19
References
1970
Year
HypertensionCardiovascular FunctionBlood PressureBlood FlowIntegrative PhysiologyVascular ReactivityAtherosclerosisResistance VesselsAssisted CirculationSodium HomeostasisVascular AdaptationAntihypertensive TherapyVascular PharmacologyCardiovascular ReactivityVascular BiologyDiuretic ResistanceSpontaneously Hypertensive RatsPharmacologyPotassium HomeostasisFlow ResistanceCardiovascular DiseasePhysiologyEndothelial DysfunctionResistance CurvesCardiovascular PhysiologyMedicine
The hindquarters of spontaneously hypertensive rats and normotensive controls were perfused at constant flow and their resistance curves compared to those of hypothetical vessels differing only in media thickness, showing that increased wall mass explains the observed resistance differences. SHR vessels display markedly higher flow resistance even at maximal dilation, steeper noradrenaline dose–response curves, and greater maximal contractile strength, indicating that an enlarged contractile wall mass reduces lumen size and accounts for the heightened resistance and reactivity without requiring increased smooth muscle activity.
Abstract The hindquarters of a spontaneously hypertensive rat (SHR) and a matched normotensive control rat (NCR) were perfused at a constant rate of flow with oxygenated plasma substitute in 15 paired experiments. As is the case in the entire systemic vascular bed (Folkow et al. 1969), flow resistance was raised even during maximal dilatation in SHR (p<0.001), almost in proportion to their raised blood pressure. Graded noradrenaline (NA) infusions showed identical NA “thresholds”, while SHR displayed a steeper curve, relating log NA dose to resistance response (p<0.001) and a greater maximal contractile strength of the resistance vessels (p<0.001). These characteristics of the resistance curves for SHR and NCR were compared with those mathematically deduced for two hypothetical vessels, identical except for the presence in one of them of a 30 per cent increase of its media thickness encroaching upon its lumen even at complete relaxation. In all essential points the relationships between the two sets of curves were the same while no other type of vascular change, structural or functional, could alone reproduce all the characteristics of the SHR curve. The results therefore suggest the presence of an increased contractile wall mass in the systemic resistance vessels of SHR encroaching upon their lumina even during maximal dilatation. Without necessitating any increased smooth muscle activity the haemodynamic effects of the proposed structural change can largely alone account for the raised resistance and increased vascular “reactivity” in SHR.
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