Smooth muscle cell types at different aortic levels and in microvasculature of rabbits with renovascular hypertension.
BACKGROUND
The monoclonal antimyosin antibodies smooth muscle (SM)-E7, non-muscle (NM)-G2 and NM-F6 recognize smooth muscle myosin heavy chains, and A- and B-like non-muscle myosin heavy chains, respectively. On this basis, aortic smooth muscle cell types have been identified as adult (SM-E7-positive), postnatal (SM-E7- and NM-G2-positive) and fetal (SM-E7-, NM-G2- and NM-F6-positive). We have demonstrated previously that hypertrophy of the smooth muscle cell layer of the upper aorta in two-kidney, one clip hypertensive rabbits is achieved via a selective increase in postnatal-type smooth muscle cells.


OBJECTIVE
To monitor the time-course change of postnatal-type smooth muscle cells along the entire aortic tree and to define the phenotypic characteristics of the microvasculature in the same rabbit model.


METHODS
Hypertensive rabbits were killed 0.5, 1, 2.5, 4, 6 and 8 months after clipping. Normotensive age-matched rabbits served as controls. The entire aorta was frozen during perfusion at a constant pressure for morphometric and immunocytochemical studies. Transverse cryosections were taken 1 cm from the aortic valve (level A), immediately after the anonymous trunk (level B), immediately before the diaphragm (level C), and near the bifurcation (level D). Small vessels and arterioles were studied in psoas skeletal muscle and in left ventricular myocardium.


RESULTS
On the whole, aortae from hypertensive rabbits displayed a striking increase in postnatal-type smooth muscle cells at all levels by 4 months of hypertension and a progressive decrease in the number of these cells to near the control value by 8 months of hypertension. A peculiar pattern of myosin heavy chain expression was found in the microvasculature. In control and in hypertensive rabbits, both at 4 and at 8 months, small vessels and arterioles were equally reactive with the three antimyosin heavy chain antibodies. This indicates a basic prevalence of fetal-type smooth muscle cells, which is little influenced by blood pressure.


CONCLUSIONS
The present data elucidate some of the basic changes which the entire aortic segment and microvasculature undergo in the present experimental model.
Institute of Clinical Medicine, University of Padua, Italy.
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P
Pauletto
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S
Da Ros
A
A
Capriani
A
A
Chiavegato
A C
AC
Pessina
S
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Sartore
D000818:Animals; D001011:Aorta / Q000378:metabolism / Q000473:pathology*; D001160:Arterioles / Q000378:metabolism / Q000473:pathology*; D002455:Cell Division; D003331:Coronary Vessels / Q000378:metabolism / Q000473:pathology*; D006352:Heart Ventricles / Q000378:metabolism / Q000473:pathology; D006978:Hypertension, Renovascular / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology*; D018995:Myosin Heavy Chains / Q000378:metabolism*; D010641:Phenotype; D016658:Psoas Muscles / Q000098:blood supply*; D011817:Rabbits
D018995:Myosin Heavy Chains