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Attenuated microvascular alterations in coarctation hypertension
1Department of Physiology, Eastern Virginia Medical School, Norfolk 23501.
Insights
Chronic hypertension causes arteriolar changes. This study in cremaster muscle suggests these alterations, including reduced diameter and density, are pressure or flow dependent, unlike in renal hypertension.
Area of Science:
- Physiology
- Vascular Biology
- Hypertension Research
Background:
- Chronic hypertension is linked to arteriolar vasoconstriction, diameter reduction, and rarefaction.
- The pressure or flow dependence of these microvascular changes in hypertension remains unclear.
Purpose of the Study:
- To investigate the pressure and flow dependence of arteriolar functional and structural changes during developing and chronic coarctation hypertension.
- To compare these alterations with those seen in renal hypertension models.
Main Methods:
- Coarctation hypertension was induced in rats using a silver clip on the abdominal aorta.
- Arteriolar diameters, vascular tone, medial-intimal area, and arteriole density were measured in the cremaster muscle at 2, 4, and 8 weeks post-intervention.
- Measurements were compared between hypertensive and control rats.
Main Results:
- Reduced resting diameters were observed in second-, third-, and fourth-order arterioles in hypertensive rats.
- Elevated vascular tone was noted in second-, third-, and fourth-order arterioles.
- No significant increase in medial-intimal area was found.
- A 20% reduction in small arteriole density occurred at 8 weeks of hypertension.
Conclusions:
- Arteriolar diameter reductions and rarefaction in coarctation hypertension are attenuated compared to one-kidney, one-clip hypertension.
- These findings suggest that microvascular alterations in hypertension are largely dependent on pressure and flow levels.
Abstract:
Arteriolar vasoconstriction, structural reductions in dilated diameter, and rarefaction have been observed in vascular beds with chronic renal hypertension. To determine their pressure or flow dependence, these functional and structural parameters were studied in the developing and chronic stages of coarctation hypertension in the cremaster muscle, a normotensive skeletal muscle bed that is protected from the effects of elevated microvascular pressures. Hypertension was produced in rats by placing a silver clip around the abdominal aorta above the branches of the renal arteries. In hypertensive rats, resting diameters were reduced in second-order arterioles after 4 and 8 wk, in third-order arterioles after 2, 4, and 8 wk, and in fourth-order arterioles after 4 and 8 wk, vs. controls. Vascular tone was elevated in second-order arterioles after 2, 4, and 8 wk and in third- and fourth-order arterioles after 8 wk in hypertensive rats. No increases in medial-intimal area were found at any stage of hypertension in any arteriolar order. The density of small arterioles (3rd-5th orders) was reduced by 20% in hypertensive rats at 8 wk but was unchanged at the other time periods. These arteriolar alterations, especially the absence of structural reductions in diameter, are attenuated compared with those observed in one-kidney, one-clip hypertension and suggest that most of the arteriolar alterations that occur in renal hypertension are pressure or flow dependent.