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Review
. 2014 May;63(5):e110-7.
doi: 10.1161/HYPERTENSIONAHA.114.02441. Epub 2014 Mar 10.

2013 Dahl Lecture: American Heart Association council for high blood pressure research clarifying the physiology of endothelin

David M Pollock  1
Affiliations
Review

2013 Dahl Lecture: American Heart Association council for high blood pressure research clarifying the physiology of endothelin

David M Pollock. Hypertension. 2014 May.
No abstract available

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Figures

Figure 1
Figure 1
Change in mean 24-hr systolic blood pressure in subjects with resistant hypertension treated with either placebo, darusentan (DAR), or guanfacine (GUAN) for 14 weeks in addition to at least three other types of anti-hypertensive medications (from Bakris et al.)
Figure 2
Figure 2
Systolic blood pressure measured by telemetry in collecting duct specific knockout (KO) mice in response to being placed on a high salt diet (adapted from a series of papers from Kohan’s laboratory–).
Figure 3
Figure 3
Hypothetical scheme for ET-1 and ETA and ETB receptor involvement in the physiological response to high salt. Sites where angiotensin II may interfere to induce salt-sensitivity are indicated by the red asterisk.
Figure 4
Figure 4
Scheme depicting the autocrine and paracrine actions of ET-1 within the renal inner medulla. Used with permission.
Figure 5
Figure 5
Potential pathways depicting the overall physiological role of ET-1 to function as a pro-natriuretic factor to regulate the sodium excretion (UNaV). The three pathways on the right are well established with sympatho-regulation and skin Na+ buffering await further confirmation.
See this image and copyright information in PMC

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