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Effects of chronic hypertension and its reversal on arteries and arterioles
1Department of Physiology, Eastern Virginia Medical School, Norfolk.
Insights
Reversing hypertension in rats normalized heart and large vessel changes, but microvascular alterations in arterioles required more time for full recovery. This highlights differing long-term adaptations in arteries versus arterioles.
Area of Science:
- Cardiovascular Physiology
- Renal Hypertension Research
- Vascular Biology
Background:
- Chronic renal hypertension causes microvascular changes.
- The reversibility of these structural and functional alterations remains unclear.
Purpose of the Study:
- To investigate the reversibility of microvascular alterations in chronic renal hypertension.
- To compare structural adaptations in arterioles and arteries following hypertension reversal.
Main Methods:
- Induction of one-kidney, one-clip hypertension in rats.
- Measurement of in vivo arteriolar and venular dimensions.
- Histological analysis of aortic and arteriolar medial-intimal hypertrophy.
- Assessment of heart weight changes.
Main Results:
- Hypertension reversal normalized aortic medial-intimal hypertrophy and heart weight.
- Arteriolar medial-intimal area and relaxed diameter reductions were only partially restored after hypertension reversal.
- Systolic blood pressure normalized rapidly after clip removal.
Conclusions:
- Reversal of chronic renal hypertension can normalize structural changes in the heart and large arteries.
- Complete normalization of arteriolar structural changes may require longer recovery periods.
- Arterioles and arteries exhibit distinct long-term structural adaptations to chronic hypertension.
Abstract:
The reversibility of functional and structural microvascular alterations in chronic renal hypertension has not been established. Twelve weeks after surgery to induce hypertension, in vivo arteriolar and venular dimensions were measured in the cremaster muscle of rats with one-kidney, one-clip hypertension (1K1C), rats in which the clip was removed after 8 weeks (1KNT), and controls. Systolic blood pressure was significantly elevated after 3 days in 1K1C rats and reached a plateau by 6 weeks. In 1KNT rats, systolic blood pressures were similar to 1K1C rats but were normalized 1 day after unclipping. A marked medial-intimal hypertrophy was found by histological techniques in the thoracic and abdominal aortae (45% and 69%, respectively) but not in cremaster feeding arteries of 1K1C rats. These arterial changes were reversed after unclipping. In 1K1C rats, medial-intimal area decreased in first- through fourth-order (1A, 2A, 3A, and 4A) arterioles along with a decline in relaxed diameter (41%, 30%, 20%, and 21%, respectively), which was only partially restored after unclipping. Heart weight was increased by 67% in 1K1C rats, but it did not differ between 1KNT and controls. Therefore, the reversal of chronic renal hypertension can normalize gross structural alterations in the heart and large vessels, but more time may be required to normalize completely the arteriolar changes. These data indicate that long-term structural adaptations in renal hypertension are different in arterioles and arteries, and they may be related to chronic changes in blood flow and/or pressure.