Arterial pressure, cardiac output and systemic resistance before and after pithing in normotensive and spontaneously hypertensive rats.

After complete cardiovascular denervation mean arterial pressure (MAP) falls to almost equally low levels in spontaneously hypertensive rats (SHR) and normotensive control rats (NCR). This has earlier been suggested to indicate a dominance of neurogenic mechanisms in established SHR hypertension. -- In the present study, total peripheral resistance (TPR) remains, however, some 35 per cent higher in adult SHR than in NCR after pithing while cardiac output (CO), and stroke volume, is 35 per cent lower in SHR. These opposite differences in TPR and CO after denervation, resulting in equal MAP levels in SHR and NCR, seem rather to be a consequence of the rapidly established structural adaptation that affects all SHR high-pressure cardiovascular sections. Thus, the SHR precapillary resistance vessels display thickened walls and luminal narrowing, which keeps TPR higher than in NCR even during maximal vasodilatation. Due to hypertrophy, the SHR left ventricle exhibits a reduced myocardial stretch for a given filling pressure and stroke volume is consequently reduced more than in NCR after complete denervation. -- Paradoxically, therefore, rather than reflecting any dominance of neurogenic mechanisms in established SHR hypertension the MAP equalization in SHR and NCR after cardiovascular denervation emphasizes the hemodynamic importance of cardiovascular structural changes present in hypertension.