Role of the sympathetic nervous system in human renovascular hypertension
- 49 Downloads
The findings in humans as to whether elevated sympathetic nerve activity contributes to renovascular hypertension have been less consistent compared with the results obtained in experimental models of renovascular hypertension. Collectively, there are several lines of evidence to support the view that sympathetic nerve activity is elevated in patients with renovascular hypertension. It is uncertain, however, whether this adrenergic overactivity is specific for renovascular hypertension per se, or the cause of severe hypertension with target organ damage. Central or peripheral stimulation of sympathetic nerve activity by angiotensin II, or stimulation of central sympathetic outflow via afferent renal nerves of ischemic kidneys, are possible mechanisms to explain the elevated sympathetic nerve activity in renovascular hypertension. Therapy that diminishes the activity of the sympathetic nervous system and the renin-angiotensin system seems rational and could perhaps also improve the poor prognosis for these patients.
Unable to display preview. Download preview PDF.
References and Recommended Reading
- 2.Johansson M, Herlitz H, Jensen G, et al.: Increased cardiovascular mortality in hypertensive patiens with renal artery stenosis. Relation to sympathetic activation, renal function and treatment regimens. J Hypertens 1999, 17:1743–1750. A study showing elevated cardiovascular mortality in patients with hypertension and renovascular disease compared with the normal population of Sweden. Elevated plasma NE concentrations did not predict an adverse prognosis and mortality remained high whether revascularization was performed or not, possibly due to concomitant coronary disease.PubMedCrossRefGoogle Scholar
- 11.Sigmon DH, Beierwaltes WH: Influence of nitric oxide in the chronic phase of two-kidney, one clip renovascular hypertension. Hypertension 1998, 31:649–656. In the chronic phase 2K-1C model of renovascular hypertension there was only a moderate reduction of blood pressure after losartan, indicating a prevailing angiotensin-independent vasoconstriction. The authors conclude that in the early and chronic phases of 2K-1C hypertension, nitric oxide contributes significantly to buffer the hypertension and maintain perfusion of both kidneys by counterbalancing vasoconstriction.PubMedGoogle Scholar
- 26.Bradley T, Hjemdahl P: Further studies on renal nerve stimulation induced release of noradrenaline and dopamin from the canine kidney in situ. Acta Physiol Scand 1984, 122:367–379.Google Scholar
- 30.Wallin B, Elam M: Insights in intraneural recordings of sympathetic nerve traffic in humans. News Physiol Sci 1994, 9:7–11.Google Scholar
- 34.Grassi G, Cattaneo BM, Seravalle G, et al.: Baroreflex control of sympathetic nerve activity in essential and secondary hypertension. Hypertension 1998, 31:68–72. The authors reported reduced MSA in secondary compared with primary hypertension. Interpretation of the data is limited by the study design where patients with pheochromocytoma and patients with renal artery stenosis were lumped together in the group of secondary hypertensives.PubMedGoogle Scholar
- 35.Johansson M, Elam M, Rundqvist B, et al.: Increased sympathetic nerve activity in renovascular hypertension. Circulation 1999, 99:2537–2542. This study provides evidence for elevated sympathetic nerve activity in patients with renal artery stenosis and hypertension. Sympathetic nerve activity was assessed by both radiotracer technique and microneurography. The diagnosis of renovascular hypertension was proven by cure or improvement of hypertension after revascularization in a subgroup of patients.PubMedGoogle Scholar
- 40.Ligtenberg G, Blankestijn PJ, Oey PL, et al.: Reduction of sympathetic hyperactivity by enalapril in patients with chronic renal failure [see comments]. N Engl J Med 1999, 340:1321–1328. This study showed elevated MSA in patients with moderately reduced renal function compared with healthy controls. Using a cross-over design, the authors showed reduced MSA after chronic treatment with an ACE inhibitor, whereas amlodipine, a calcium channel blocker, increased MSA.PubMedCrossRefGoogle Scholar
- 44.Yusuf S, Sleight P, Pogue J, et al.: Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators [see comments]. N Engl J Med 2000, 342:145–153. Important study showing reduced rates of death, myocardial infarction, and stroke in a broad range of high-risk patients who did not have known low left ventricular ejection fraction or heart failure. The results are relevant to patients with renovascular hypertension who present similar clinical characteristics as the population of the HOPE study.PubMedCrossRefGoogle Scholar
- 46.Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL randomised intervention trial in congestive heart failure (MERIT-HF) [see comments]. Lancet 1999, 353:2001–2007.Google Scholar