Evidence of Renin Release or Production in Splanchnic Territory

Ganten, Detlev; Hayduk, K; Brecht, H. M.; Boucher, R.; Genest, Jacques

doi:10.1038/226551a0

Cited by 77 publications

(31 citation statements)

References 6 publications

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“…7 -8 Such renin-like activity has been demonstrated in arteries and veins of hog, rat, and dog. 7 ' 10 The enzyme appears to be similar to kidney renin and it has been suggested that it is transported to blood vessels from plasma. 8 More recently, however, the demonstrations that renin activity is present in mesenteric vessels of dogs 24 hours after nephrectomy, and that this activity increases after severe hemorrhage, 10 appear to indicate that the enzyme is synthesized locally in blood vessels.…”

Section: Discussionmentioning

confidence: 99%

“…7 ' 10 The enzyme appears to be similar to kidney renin and it has been suggested that it is transported to blood vessels from plasma. 8 More recently, however, the demonstrations that renin activity is present in mesenteric vessels of dogs 24 hours after nephrectomy, and that this activity increases after severe hemorrhage, 10 appear to indicate that the enzyme is synthesized locally in blood vessels. These observations and the demonstration that renin cannot release A II directly from tetradecapeptide renin substrate 25 suggest that the facilitatory effect of renin substrate on the adrenergic neuroeffector unit is mediated by the generation of A I, which subsequently was converted to A II within the vascular tissue.…”

Section: Discussionmentioning

confidence: 99%

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Facilitation of adrenergic transmission by locally generated angiotensin II in rat mesenteric arteries.

Malik

Nasjletti

1976

Circulation Research

206

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When studied on isolated rat mesenteric arteries perfused with Tyrode's solution, angiotensin I and angiotensin 11(1 ng/ml), a synthetic tetradecapeptide renin substrate, and a purified hog renin substrate (50-100 ng/ml) potentiated vasoconstrictor responses to sympathetic nerve stimulation and to injected norepinephrine without altering basal pressure. These agents produced a greater augmentation of the vasoconstrictor responses to nerve stimulation than to injected norepinephrine. The potentiation of vasoconstrictor responses to sympathetic nerve stimulation and injected norepinephrine which was elicited by renin substrate and angiotensin I was abolished by an inhibitor of angiotensin I-converting enzyme, SQ 20,881, and by an angiotensin II receptor antagonist, [Sar'-Ile 8 ]angiotensin II. In contrast, the potentiating effect of angiotensin II was blocked only by the latter compound. We conclude that utilization of renin substrate within the vascular wall by renin or renin-like enzymes results in the formation of angiotensin I, which is converted to angiotensin II. Angiotensin in turn potentiates the vasoconstrictor responses to adrenergic stimuli presumably by augmenting release of the adrenergic transmitter and inhibiting its neuronal reuptake as well as by increasing vascular reactivity to norepinephrine. ANGIOTENSIN II (A II), in addition to exerting a potent vasoconstrictor effect, enhances sympathetic activity in several tissues innervated by adrenergic nerves where it augments the response to sympathetic nerve stimulation as well as to injected norepinephrine. 1 Facilitation of adrenergic nervous effects by A II appears to be due to enhanced synthesis 2 and release, 3 ' 5 as well as to inhibition of neuronal reuptake, of norepinephrine. 8 The demonstration of the presence of angiotensin-forming enzymes (renin, angiotensin I-converting enzyme) in extrarenal tissues including blood vessels 7 " 12 raises the possibility that A II formed locally within vascular tissues modulates adrenergic nervous activity. To test this hypothesis we have examined the effect, in rat mesenteric arteries perfused with Tyrode's solution, of natural and synthetic (tetradecapeptide) renin substrates and of both A I and A II on vasoconstrictor responses to periarterial nerve stimulation and to injected norepinephrine. To distinguish direct effects of the precursors of A II from those produced by local generation of A II within the vascular tissue, we have investigated the action of these agents on the vasoconstrictor responses to adrenergic stimuli after blockade of the activity of the renin-angiotensin system with either (1) an inhibitor of A I-converting enzyme, SQ 20,881" or (2) a competitive antagonist of A II, [Sar^Ile 8 ]-angiotensin II. 14 The effect of A II and other agents on the vasoconstrictor responses to periarterial nerve stimulation described in this study is presumed to be due to their action on the adrenergic neuromuscular junction, since the work of McGregor 15 and our previous observations 16 indicate ...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Facilitation of adrenergic transmission by locally generated angiotensin II in rat mesenteric arteries.

Malik

Nasjletti

1976

Circulation Research

206

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“…Renin-like activity was found early in vessel homogenates (200) . Interest in vascular renin was revived when renin-like activity in some resistance vessels was shown to persist up to 12 days after bilateral nephrectomy in dialyzed dogs (201). Vascular renin even increased in these nephrectomized animals following hemorrhage, as did plasma renin.…”

Section: Vasculaturementioning

confidence: 98%

The Role of the Renin-Angiotensin System in Cardiovascular Disease.

et al. 1994

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Recent findings have increased our understanding of the role of the renin-angiotensin system in cardiovascular diseases. This was possible by the progress made in molecular biology and the import of this methodology into cardiovascular research by several groups in the past few years. Studies by these groups accumulated evidence especially for the existence and physiological importance of organ-based renin-angiotensin systems and their involvement in the pathogenesis of hypertension and the accompanying disorders of the heart, the kidney, and the vessels. This Review will focus mainly on the relevance of the local renin-angiotensin systems for cardiovascular diseases and the value of transgenic animals as models to analyse these systems (Hypertens Res 1994; 17: 1-16).

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“…Since its founding, 25 years have passed and the MDC has performed even beyond Detlev Ganten's expectations. Of course, since his first two publications appeared in Nature [1] and in Science [2], he probably believes that such publications are easy, as they were for him.…”

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confidence: 99%

A visionary scientist selects clinicians for clinical research

Luft

2016

J Mol Med

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We celebrate Detlev Ganten's 75th birthday late this March (Fig. 1); we hope he is celebrating too. Detlev Ganten is not only founding editor of the Journal of Molecular Medicine and still active in this capacity, he is also the initial director of the Max-Delbrück Center for Molecular Medicine (MDC) Berlin-Buch. The MDC traces its heritage to the KaiserWilhelm Institute für Hirnforschung, officially founded 1931. The collaboration between Nikolai TimofejewRessovsky, Karl Zimmer, and Max Delbrück that resulted in placing genetics on a molecular footing has been told many times. When the institute was reconstituted after German reunification, Detlev Ganten was given the task of resurrecting the MDC to world-class. And so he did; for 13 years, he was at the helm. Since its founding, 25 years have passed and the MDC has performed even beyond Detlev Ganten's expectations. Of course, since his first two publications appeared in Nature [1] and in Science [2], he probably believes that such publications are easy, as they were for him.Detlev Ganten gave the MDC a unique mission, namely pursuing the highest caliber of disease-oriented (clinical) biological research focusing on the basic mechanisms and molecules of relevance in health and disease and emphasizing the most advanced methodologies in cell biology, genetics, and genomics. He was less interested in the topic and wisely supported the idea that the MDC should pursue a broad spectrum of problems comprising the current chronic scourges, namely cardiovascular disease, cancer, and neurodegenerative disorders. Similarly circumspect, the MDC has maintained this broad base until the present day.Another unique decision Detlev Ganten made was to include clinicians in the field of MDC senior scientists. As the institute had a tradition of encompassing clinical departments since the time of Oskar and Cécile Vogt, the decision was made easier. The institute had continued that tradition and before German reunification had worked intensively with a clinic dedicated to cancer and a clinic for cardiovascular diseases in the framework of the BAcademy of the Sciences^. However, although the clinics were still there, the framework was gone and to continue the concept in conjunction with the two medical schools Berlin had in 1991 was difficult. Furthermore, the mission Detlev Ganten espoused was not necessarily commensurate with the usual department chairmanships in academic medicine. Clinical excellence, teaching, and research were the appropriate criteria of the time; however, Detlev Ganten wanted the order and emphasis revised and reversed. Research at an internationally competitive level was to receive priority, yet the clinical departments also had to work; the patient care had to be excellent, and the teaching mission was not to be ignored. He found his clinicians and the search also underscores the value of personal relationships when making personnel decisions.

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Evidence of Renin Release or Production in Splanchnic Territory

Cited by 77 publications

References 6 publications

Facilitation of adrenergic transmission by locally generated angiotensin II in rat mesenteric arteries.

Facilitation of adrenergic transmission by locally generated angiotensin II in rat mesenteric arteries.

The Role of the Renin-Angiotensin System in Cardiovascular Disease.

A visionary scientist selects clinicians for clinical research

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