Hypertension II: Hypertension and Vascular Control


Re: Arteriolar responsiveness in angiotensin II-induced hypertension

John D. Imig
jdimig@mailhost.tcs.tulane.edu


On Thu Dec 10, Matt Boegehold wrote
-----------------------------------
>Dr. Imig,
>This is a very nice study. It is interesting to me that myogenic responsiveness is unaltered in interlobular and afferent arterioles of the rats made hypertensive by AII infusion. In light of previous reports that sub-pressor concentrations of norepinephrine can enhance arteriolar myogenic responses in rat cremaster muscle, do you think that normal, relatively low circulating levels of AII in vivo could also exert some continuous enhancing effect on myogenic activity? Of course, it may be that any such enhancement would only occur if the vessel were exposed to the AII at the time the myogenic stimulus were applied, which would not be the case if the vessel were being perfused in-vitro. What do you think?

>Matt Boegehold


Dr. Boegehold,

In the current set of experiments it is very difficult to separate the actions of  chronic angiotensin II infusion from the elevation in mean arterial pressure.  Previous studies have demonstrated that in normotensive animals the afferent arteriolar response to increases in renal perfusion pressure is not significantly altered by the presence of angiotensin II. Interestingly, the tubuloglomerular feedback response, which influences primarily the distal portion of the afferent arteriole, is enhanced during acute elevations of circulating angiotensin II levels.

Additionally, we have done a more thorough evaluation of the afferent arteriolar response to increases in perfusion pressure during various time points in the development of angiotensin II-induced hypertension. We have observed an impairment of the afferent arteriolar autoregulatory response after one week of angiotensin II infusion which starts to improve at 10 days and is similar to normotensive animals by two weeks (Abstract, J Am Soc Nephrol 9:308A, 1998).  This would suggest that the renal microvasculature is adapting to the elevated blood pressure and/or angiotensin II levels to properly control renal blood flow and glomerular filtration.

John D. Imig


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