Surgically Induced Hypertension

One of the major discoveries in hypertension research in the twentieth century was that of Goldblatt and his associates in 1937. They occluded the main renal artery of one kidney in six dogs and found that renin levels in the peripheral blood of these animals substantially increased. Over the next 3-4 days the mean systemic blood pressure in these animals also increased by an average of 104-139 mmHg. The Goldblatt technique was later used in rats and more recently in mice and led to the establishment of models with transient or permanent renal artery occlusion with or without unilateral nephrectomy. These models are referred to as two kidneys/one clip (2K1C) or one kidney/one clip (1K1C) hypertension models. The initial phase of hypertension in either of these models is associated with a rapid increase in plasma renin levels and a subsequent increase in Ang II formation. In the 2K1C model, the RAS remains activated for at least 9 weeks after occlusion of the renal artery. After a few weeks the 1K1C model becomes a model of low-renin, volume-dependent hypertension, since volume retention by a single kidney tends to inhibit renin secretion.14

Eventually, however, the 2K1C rat model tends to develop volume-dependent hypertension. In the 2K1C mouse model, Ang II produces and maintains hypertension by activating the AT1A receptor subtype, while nitric oxide (NO) seems to counteract the hypertensive effects of Ang II.15

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