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Amino acids that centrally influence blood pressure and regional blood flow in conscious rats.

Takemoto Y - J Amino Acids (2012)

Bottom Line: This paper firstly describes why amino acids are selected and outlines how the brain regulates blood pressure and regional blood flow.Thereafter, cardiovascular actions of some of amino acids at the mechanism level will be discussed based upon findings of pharmacological and regional blood flow measurements.Several examined amino acids in addition to the established neurotransmitter amino acids appear to differentially activate brain structures to produce changes in blood pressure and regional blood flows.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurophysiology, Graduate School Biomedical Sciences, Hiroshima University, Kasumi-cho 1-2-3, Minami-ku, Hiroshima, 734-8551, Japan.

ABSTRACT
Functional roles of amino acids have increasingly become the focus of research. This paper summarizes amino acids that influence cardiovascular system via the brain of conscious rats. This paper firstly describes why amino acids are selected and outlines how the brain regulates blood pressure and regional blood flow. This section includes a concise history of amino acid neurotransmitters in cardiovascular research and summarizes brain areas where chemical stimulations produce blood pressure changes mainly in anesthetized animals. This is followed by comments about findings regarding several newly examined amino acids with intracisternal stimulation in conscious rats that produce changes in blood pressure. The same pressor or depressor response to central amino acid stimulations can be produced by distinct mechanisms at central and peripheral levels, which will be briefly explained. Thereafter, cardiovascular actions of some of amino acids at the mechanism level will be discussed based upon findings of pharmacological and regional blood flow measurements. Several examined amino acids in addition to the established neurotransmitter amino acids appear to differentially activate brain structures to produce changes in blood pressure and regional blood flows. They may have physiological roles in the healthy brain, but pathological roles in the brain with cerebral vascular diseases such as stroke where the blood-brain barrier is broken.

No MeSH data available.


Related in: MedlinePlus

Potential pathways between the central nervous system (CNS) and the cardiovascular system. The CNS regulates the cardiovascular system using various peripheral routs. Arterioles can be regulated by sympathetic neurons and humoral factors of angiotensin II (A II), vasopressin (VP), and adrenaline (Adr), resulting in changes in total peripheral resistance. The heart is regulated by both of parasympathetic and sympathetic neurons and Adr. Capacitance venous vessels are regulated by sympathetic neurons and modify returning blood volume to the heart and cardiac output as predicted by Starling's law. Renal sympathetic neurons can release the enzyme renin from the juxtaglomerular apparatus into the blood via β1 adrenoceptors. The renin produces A II via the renin-angiotensin system. The hypothalamus-pituitary system in the forebrain releases VP into the stream. A II and VP constrict arterioles markedly. Adrenal sympathetic neurons release Adr into the blood. The central nervous system monitors arterial blood pressure with visceral afferents terminated in the big arteries. Ach: acetylcholine, Nor: noradrenaline. circles 1–4; see text.
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fig4: Potential pathways between the central nervous system (CNS) and the cardiovascular system. The CNS regulates the cardiovascular system using various peripheral routs. Arterioles can be regulated by sympathetic neurons and humoral factors of angiotensin II (A II), vasopressin (VP), and adrenaline (Adr), resulting in changes in total peripheral resistance. The heart is regulated by both of parasympathetic and sympathetic neurons and Adr. Capacitance venous vessels are regulated by sympathetic neurons and modify returning blood volume to the heart and cardiac output as predicted by Starling's law. Renal sympathetic neurons can release the enzyme renin from the juxtaglomerular apparatus into the blood via β1 adrenoceptors. The renin produces A II via the renin-angiotensin system. The hypothalamus-pituitary system in the forebrain releases VP into the stream. A II and VP constrict arterioles markedly. Adrenal sympathetic neurons release Adr into the blood. The central nervous system monitors arterial blood pressure with visceral afferents terminated in the big arteries. Ach: acetylcholine, Nor: noradrenaline. circles 1–4; see text.

Mentions: Stimulation of central nervous system influences arterioles and/or blood pressure through at least four ways (Figure 4) [39]: one is the vasomotor sympathetic neurons in different vascular beds (Figures 2 and 4 circle 1), second is renal sympathetic neurons (Figure 4 circle 2) that release the enzyme renin from the renin-secreting granular cells in the afferent arteriole to finally produce a potent vasoactive peptide, angiotensin II, in the blood via the renin-angiotensin system [40, 41], third is adrenal sympathetic neurons (Figure 4 circle 3) that release adrenaline into the blood [42], and finally the hypothalamus-pituitary system that releases the vasoactive or antidiuretic peptide, vasopressin, in the blood (Figure 4 circle 4) [19]. Central excitatory stimulation of those pathways induces a simple pressor response through vasoconstriction by noradrenaline, angiotensin II, and vasopressin and/or increase in cardiac output with adrenaline, but inhibitory stimulation produces a depressor response where the corresponding tonic pathway at rest is deactivated. Because total vascular tone is mainly maintained by vasomotor sympathetic neurons in the animal with normal blood pressure, responses of regional blood flow resistances to inhibitory stimulation would affect vascular beds which are tonic at rest and responsible for maintaining the normal blood pressure. In the same way, genetically or experimentally produced hypertensive animals could be examined with blockade of the above-mentioned four possible peripheral pathways to elucidate the cause of prolonged hypertensive states.


Amino acids that centrally influence blood pressure and regional blood flow in conscious rats.

Takemoto Y - J Amino Acids (2012)

Potential pathways between the central nervous system (CNS) and the cardiovascular system. The CNS regulates the cardiovascular system using various peripheral routs. Arterioles can be regulated by sympathetic neurons and humoral factors of angiotensin II (A II), vasopressin (VP), and adrenaline (Adr), resulting in changes in total peripheral resistance. The heart is regulated by both of parasympathetic and sympathetic neurons and Adr. Capacitance venous vessels are regulated by sympathetic neurons and modify returning blood volume to the heart and cardiac output as predicted by Starling's law. Renal sympathetic neurons can release the enzyme renin from the juxtaglomerular apparatus into the blood via β1 adrenoceptors. The renin produces A II via the renin-angiotensin system. The hypothalamus-pituitary system in the forebrain releases VP into the stream. A II and VP constrict arterioles markedly. Adrenal sympathetic neurons release Adr into the blood. The central nervous system monitors arterial blood pressure with visceral afferents terminated in the big arteries. Ach: acetylcholine, Nor: noradrenaline. circles 1–4; see text.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3368589&req=5

fig4: Potential pathways between the central nervous system (CNS) and the cardiovascular system. The CNS regulates the cardiovascular system using various peripheral routs. Arterioles can be regulated by sympathetic neurons and humoral factors of angiotensin II (A II), vasopressin (VP), and adrenaline (Adr), resulting in changes in total peripheral resistance. The heart is regulated by both of parasympathetic and sympathetic neurons and Adr. Capacitance venous vessels are regulated by sympathetic neurons and modify returning blood volume to the heart and cardiac output as predicted by Starling's law. Renal sympathetic neurons can release the enzyme renin from the juxtaglomerular apparatus into the blood via β1 adrenoceptors. The renin produces A II via the renin-angiotensin system. The hypothalamus-pituitary system in the forebrain releases VP into the stream. A II and VP constrict arterioles markedly. Adrenal sympathetic neurons release Adr into the blood. The central nervous system monitors arterial blood pressure with visceral afferents terminated in the big arteries. Ach: acetylcholine, Nor: noradrenaline. circles 1–4; see text.
Mentions: Stimulation of central nervous system influences arterioles and/or blood pressure through at least four ways (Figure 4) [39]: one is the vasomotor sympathetic neurons in different vascular beds (Figures 2 and 4 circle 1), second is renal sympathetic neurons (Figure 4 circle 2) that release the enzyme renin from the renin-secreting granular cells in the afferent arteriole to finally produce a potent vasoactive peptide, angiotensin II, in the blood via the renin-angiotensin system [40, 41], third is adrenal sympathetic neurons (Figure 4 circle 3) that release adrenaline into the blood [42], and finally the hypothalamus-pituitary system that releases the vasoactive or antidiuretic peptide, vasopressin, in the blood (Figure 4 circle 4) [19]. Central excitatory stimulation of those pathways induces a simple pressor response through vasoconstriction by noradrenaline, angiotensin II, and vasopressin and/or increase in cardiac output with adrenaline, but inhibitory stimulation produces a depressor response where the corresponding tonic pathway at rest is deactivated. Because total vascular tone is mainly maintained by vasomotor sympathetic neurons in the animal with normal blood pressure, responses of regional blood flow resistances to inhibitory stimulation would affect vascular beds which are tonic at rest and responsible for maintaining the normal blood pressure. In the same way, genetically or experimentally produced hypertensive animals could be examined with blockade of the above-mentioned four possible peripheral pathways to elucidate the cause of prolonged hypertensive states.

Bottom Line: This paper firstly describes why amino acids are selected and outlines how the brain regulates blood pressure and regional blood flow.Thereafter, cardiovascular actions of some of amino acids at the mechanism level will be discussed based upon findings of pharmacological and regional blood flow measurements.Several examined amino acids in addition to the established neurotransmitter amino acids appear to differentially activate brain structures to produce changes in blood pressure and regional blood flows.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurophysiology, Graduate School Biomedical Sciences, Hiroshima University, Kasumi-cho 1-2-3, Minami-ku, Hiroshima, 734-8551, Japan.

ABSTRACT
Functional roles of amino acids have increasingly become the focus of research. This paper summarizes amino acids that influence cardiovascular system via the brain of conscious rats. This paper firstly describes why amino acids are selected and outlines how the brain regulates blood pressure and regional blood flow. This section includes a concise history of amino acid neurotransmitters in cardiovascular research and summarizes brain areas where chemical stimulations produce blood pressure changes mainly in anesthetized animals. This is followed by comments about findings regarding several newly examined amino acids with intracisternal stimulation in conscious rats that produce changes in blood pressure. The same pressor or depressor response to central amino acid stimulations can be produced by distinct mechanisms at central and peripheral levels, which will be briefly explained. Thereafter, cardiovascular actions of some of amino acids at the mechanism level will be discussed based upon findings of pharmacological and regional blood flow measurements. Several examined amino acids in addition to the established neurotransmitter amino acids appear to differentially activate brain structures to produce changes in blood pressure and regional blood flows. They may have physiological roles in the healthy brain, but pathological roles in the brain with cerebral vascular diseases such as stroke where the blood-brain barrier is broken.

No MeSH data available.


Related in: MedlinePlus