[Angiogenesis and arteriogenesis are increased in the SHR at the pre-hypertensive stage]

A microvascular rarefaction by angiogenic deficiency could promote the onset of hypertension in SHR, in young hypertensive patients and in normotensive descendants of hypertensive parents. We studied the angiogenic potency in prehypertensive SHR, in fibrin chambers implanted in rats, an in vivo model of angiogenesis.

Four-week pre-hypertensive SHR (n=9) and controls WKY (n=9) were implanted with fibrin gel chambers. The chamber is a cylinder (dia.: 13 mm; H: 5 mm) whose base is perforated with 10 holes of 0.8 mm. The chambers are filled with rat fibrin and implanted (n=4) into the rat dorsal subcutaneous space. After 14 days, vasculo-conjunctive buds have invaded the fibrin gel through the holes and the chambers are removed, fixed and coloured. The intact vascular buds were studied using optical microscopy. The number of vessels counted in central field corresponds to the vascular pedicle, the average number of vessels counted in 3 peripheral fields, represents the vascular branching. The number of arterialised vessels including at least 2 layers of SMC was counted in the central field of each bud.

Both rat strains remained normotensive all along the experiment. In SHR fibrin chambers, the number of peripheral vessels (20 +/- 2.6 vs 9.5 +/- 3; p<0.0001) and the number of central arterialized vessels (7.5 +/- 2 vs 2.1 +/- 1.3; p<0.0001) was significantly higher compared to WKY.

Angiogenesis and arteriogenesis are increased in pre-hypertensive SHR compared to WKY. These results plead against a microvascular rarefaction hypothesis in these genetically hypertensive rats.