Antihypertensive Drugs and the Nervous System: Ace-Inhibitors Restore Oscillatory Potentials in Hypertensives

Abstract

The authors have previously reported that oscillatory potentials (O.P.) of the electroretinogram are impaired in essential hypertensive patients before the appearance of funduscopic changes. They can therefore be considered an early marker of the nervous damage induced by hypertension. Aim of this study was to evaluate whether an antihypertensive regimen could influence the progression of this damage. O.P. were recorded in 35 essential hypertensives before antihypertensive treatment and after one-year treatment. The patients were randomly allocated into 4 treatment groups: 1) beta-blockers 2) ACE-Inhibitors 3) calcium antagonists 4) no pharmacological treatment. At the end of the study, blood pressure was significantly decreased in all but group 4. O.P., similar in the 4 groups at the beginning, were significantly higher at the end of the study only in patients treated with ACE-inhibitors. The results of this study suggest that although all hypotensive agents reduced blood pressure only ACE-I showed a protective effect on the retinal electric electrophysiology in hypertensive patients.

ACE inhibition salvages the visual loss caused by diabetes

“…In support of this contention, improvement of oscillatory potential deficits was only achievable using an ACE inhibitor, despite similar reductions in blood pressure with a calcium antagonist and a beta-blocker [35]. Instead, we posit that the effect involves an altered Na + -K + ATPase activity in the diabetic retina [34].…”

Angiotensin I–Converting Enzyme Antisense Gene Therapy Causes Permanent Antihypertensive Effects in the SHR

“…The animals were lightly anesthetized with methoxyflurane (Metofane, Mallinckrodt Veterinary, Inc). They were injected with 10 L, via cardiac route, of either physiological saline (control) or 5ϫ10 8 colony-forming units of viral particles containing LNSV-ACE-tS (viral control) or LNSV-ACE-AS (experimental) as described previously. [13][14][15][16] Polybrene (Sigma Chemical Co) at a concentration of 7 mg/mL was added to the viral medium before injection.…”

“…4 -6 This conclusion is based on the fact that the traditional pharmacological therapies targeted to inhibit the activity of the RAS are a highly successful strategy for the treatment and management of this disease in a significant population of hypertensive patients. [7][8][9][10] Despite their success, traditional pharmacological agents, such as angiotensin I-converting enzyme inhibitors (ACE-I) and the AT 1 receptor (AT 1 R) antagonists, have major limitations that include compliance, side effects, and relatively short duration of antihypertensive effects. 11,12 As a result of these limitations, the current therapeutic strategy has reached a plateau, and conceptually innovative and novel approaches must be explored to advance the field of hypertension therapies.…”

Angiotensin I–Converting Enzyme Antisense Prevents Altered Renal Vascular Reactivity, but Not High Blood Pressure, in Spontaneously Hypertensive Rats

“…The animals were lightly anesthetized with methoxyflurane (Metophane, Pittman-Moore). They were injected with 10 L, via cardiac route, of either physiological saline (control), 2ϫ10 8 colony-forming units of viral particles containing ACE-tS (viral control), or ACE-AS (experimental), as described previously. [13][14][15][16] WKY and SHR parents who were treated with either ACE-tS or ACE-AS at 5 days of age were used for breeding.…”

“…4 -6 This is based on the fact that pharmacological interruption in the activity of the RAS has proven to be highly successful in the treatment and management of hypertension in a significant population of hypertensive patients. [7][8][9][10] However, this pharmacological intervention has major limitations, which include compliance, side effects, and relatively short duration of antihypertensive effects. 11,12 As a result of these limitations, we have begun to use an antisense (AS) gene therapy approach to determine whether targeting RAS at a genetic level would be a step forward in the long-term control of hypertension.…”