Aggression-provoked huge release of submaxillary mouse renin to saliva

Pedersen, E. B.; Poulsen, Knud

doi:10.1530/acta.0.1040510

Cited by 17 publications

(4 citation statements)

References 2 publications

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“…These stimuli include stress induced by male aggressive behavior. 29 High renin concentration is probably responsible for the lower plasma levels in TG101 mice, even though these animals carry more transgene copies. PRA depends on the levels of both renin and AGT.…”

Section: Discussionmentioning

confidence: 99%

Blood Pressure–Independent Cardiac Hypertrophy Induced by Locally Activated Renin-Angiotensin System

et al. 1998

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Abstract-Cardiac hypertrophy is frequent in chronic hypertension. The renin-angiotensin system, via its effector angiotensin II (Ang II), regulates blood pressure and participates in sustaining hypertension. In addition, a growing body of evidence indicates that Ang II acts also as a growth factor. However, it is still a matter of debate whether the trophic effect of Ang II can trigger cardiac hypertrophy in the absence of elevated blood pressure. To address this question, transgenic mice overexpressing the rat angiotensinogen gene, specifically in the heart, were generated to increase the local activity of the renin-angiotensin system and therefore Ang II production. These mice develop myocardial hypertrophy without signs of fibrosis independently from the presence of hypertension, demonstrating that local Ang II production is important in mediating the hypertrophic response in vivo. (Hypertension. 1998;31:1324-1330.)

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Section: Discussionmentioning

confidence: 99%

Blood Pressure–Independent Cardiac Hypertrophy Induced by Locally Activated Renin-Angiotensin System

et al. 1998

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“…What such conditions are remains a matter of speculation. If the nerves inducing kallikrein secretion in cats function during active aggression, as has been proposed with respect to the secretion of renin in mice by Pedersen & Poulsen (1983), this may serve to make bite wounds more painful. Other possibilities in the behaviour of the animal that may require a sudden increase in kallikrein output include grooming, sexual activity, licking of new-born offspring or a special gastro-enteric function not so far appreciated.…”

Section: Discussionmentioning

confidence: 99%

Factors Affecting the Secretion of Submandibular Salivary Kallikrein in Cats

et al. 1987

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SUMMARYGlandular kallikrein has been assessed in submandibular saliva, homogenates and plasma by the fluorimetric substrate D-Val-Leu-Arg-7-amino-4-trifluoromethylcoumarin (AFC) and histochemically in tissue sections by the 4-methoxy-2-naphthylamide (MNA) analogue. Nerve stimulation was used to produce salivary secretion. Parasympathetic saliva contained low concentrations of kallikrein, independently of any circulating catecholamines from the adrenals. Sympathetic saliva contained very high concentrations of kallikrein; the amounts in individual drops rapidly reached a peak then declined gradually. Adrenergic blocking drugs during mixed parasympathetic and sympathetic stimulation showed that /J-adrenergic effects normally increase the secretion of kallikrein in response to the a-adrenergic influence from sympathetic nerve impulses. Small amounts of a glandular kallikrein-like activity are present in the plasma. Effluent blood from the submandibular gland before, during and after stimulation of either nerve gave no indication that submandibular kallikrein passes from the glandular compartment to the blood under conditions of unobstructed salivary flow. Excision of the chorda tympani indicated that parasympathetic nerve impulses are required for the normal resynthesis of submandibular kallikrein. The secretion of salivary kallikrein is essentially an exocrine function but its role in the saliva remains obscure. The results suggest that sudden mobilization of kallikrein may occur at times into the saliva and that a separate population of adrenergic axons, under separate central control, may pass to the striated ducts specially for this purpose.

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“…Ren-2 is mainly expressed in the salivary gland of males and is dramatically stimulated by aggression (100,000-fold higher levels in saliva than plasma) [46]. Possibly, the aspartyl protease serves to injure a bitten opponent or conceivably the protease serves a protective function for wound healing after a fight by wound licking.…”

Section: Dna Sequence Analysis Of An Ancient Systemmentioning

confidence: 99%

Emergence and evolution of the renin–angiotensin–aldosterone system

et al. 2012

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The renin–angiotensin–aldosterone system (RAAS) is not the sole, but perhaps the most important volume regulator in vertebrates. To gain insights into the function and evolution of its components, we conducted a phylogenetic analysis of its main related genes. We found that important parts of the system began to appear with primitive chordates and tunicates and that all major components were present at the divergence of bony fish, with the exception of the Mas receptor. The Mas receptor first appears after the bony-fish/tetrapod divergence. This phase of evolutionary innovation happened about 400 million years ago. We found solid evidence that angiotensinogen made its appearance in cartilage fish. The presence of several RAAS genes in organisms that lack all the components shows that these genes have had other ancestral functions outside of their current role. Our analysis underscores the utility of sequence comparisons in the study of evolution. Such analyses may provide new hypotheses as to how and why in today's population an increased activity of the RAAS frequently leads to faulty salt and volume regulation, hypertension, and cardiovascular diseases, opening up new and clinically important research areas for evolutionary medicine.Electronic supplementary materialThe online version of this article (doi:10.1007/s00109-012-0894-z) contains supplementary material, which is available to authorized users.

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Aggression-provoked huge release of submaxillary mouse renin to saliva

Cited by 17 publications

References 2 publications

Blood Pressure–Independent Cardiac Hypertrophy Induced by Locally Activated Renin-Angiotensin System

Blood Pressure–Independent Cardiac Hypertrophy Induced by Locally Activated Renin-Angiotensin System

Factors Affecting the Secretion of Submandibular Salivary Kallikrein in Cats

Emergence and evolution of the renin–angiotensin–aldosterone system

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