2017
DOI: 10.1097/fjc.0000000000000458
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Hypertension's 3 Dilemmas and 3 Solutions: Pharmacology of the Kidney in Hypertension

Abstract: SUMMARY The Hypertension Community has three conflicting dilemmas, a goal systolic pressure of 120 mmHg or less (The SPRINT Trials), 40% of our 60,000,000 hypertensives still sustain blood pressures above 140/90 mmHg and our most potent antihypertensive drug minoxidil sits on the side-lines, imprisoned in the FDA’s Black Box Designation. My solutions to these dilemmas are: #1. Review of the facts of our most potent antihypertensive drug minoxidil which is essentially free of toxicity, #2. Treatment focus on th… Show more

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Cited by 3 publications
(6 citation statements)
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“…Our motivation for examining the role of adenosine receptors in Dahl SS rats over a wide range of dietary salt levels (0.3%, 4%, and 8% salt diets) is that in humans there is a “dose-response” curve for dietary sodium intake versus arterial blood pressure that extends over a wide range (0.1 to 10 grams per day) of dietary sodium intake (see Figure 5 of article by Pettinger 59 ). The current study indicates that the protection against salt-diet induced hypertension afforded to females by knocking out A 1 or A 2B receptors is lost at very high levels (8%) of dietary salt.…”
Section: Discussionmentioning
confidence: 99%
“…Our motivation for examining the role of adenosine receptors in Dahl SS rats over a wide range of dietary salt levels (0.3%, 4%, and 8% salt diets) is that in humans there is a “dose-response” curve for dietary sodium intake versus arterial blood pressure that extends over a wide range (0.1 to 10 grams per day) of dietary sodium intake (see Figure 5 of article by Pettinger 59 ). The current study indicates that the protection against salt-diet induced hypertension afforded to females by knocking out A 1 or A 2B receptors is lost at very high levels (8%) of dietary salt.…”
Section: Discussionmentioning
confidence: 99%
“…From a public health viewpoint, the causal role of altered α 2 -AR regulation in hypertension via retention of excess sodium appears very promising. Millions of people ingesting 20 times the real minimum daily requirement for sodium [33] have no hypertension which is obviously genetically determined; they are salt-resistant. A drug which would convert salt-sensitive hypertension to salt-resistance by interfering selectively with the α 2 -AR-sodium retaining mechanism could be paradigm shifting.…”
Section: Resultsmentioning
confidence: 99%
“…However, when the sympathetic nervous system is reflexly activated by peripheral acting antihypertensive drugs, β-adrenoceptor blockade of excess renin release is a powerful blood pressure lowering mechanism [26][27][28]. Extensive blood pressure lowering in severely hypertensive patients leads to passive tubular retention of sodium that can be overpowering leading to severe edema, even cardiac tamponade [32], details of which are described by Pettinger [33]. Moreover, severe preglomerular arteriolar hypertrophy coupled with the magnitude of blood pressure reduction decreases glomerular filtration rate causing uremia.…”
Section: Hypertensionmentioning
confidence: 99%
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