Effects of Terpenes and Terpenoids of Natural Occurrence in Essential Oils on Vascular Smooth Muscle and on Systemic Blood Pressure: Pharmacological Studies and Perspective of Therapeutic Use

Terpenes are a class of chemical compounds with carbon and hydrogen atoms in their structure. They can be classified into several classes according to the quantity of isoprene units present in its structure. Terpenes can have their structure modified by the addition of various chemical radicals. When these molecules are modified by the addition of atoms other than carbon and hydrogen, they become terpenoids. Terpenes and terpenoids come from the secondary metabolism of several plants. They can be found in the leaves, fruits, stem, flowers, and roots. The concentration of terpenes and terpenoids in these organs can vary according to several factors such as the season, collection method, and time of the day. Several biological activities and physiological actions are attributed to terpenes and terpenoids. Studies in the literature demonstrate that these molecules have antioxidant, anticarcinogenic, anti-inflammatory, antinociceptive, antispasmodic, and antidiabetogenic activities. Additionally, repellent and gastroprotective activity is reported. Among the most prominent activities of monoterpenes and monoterpenoids are those on the cardiovascular system. Reports on literature reveal the potential effect of monoterpenes and monoterpenoids on systemic blood pressure. Studies show that these substances have a hypotensive and bradycardic effect. In addition, the inotropic activity, both positive and negative, of these compounds has been reported. Studies also have shown that some monoterpenes and monoterpenoids also have a vasorelaxing activity on several vascular beds. These effects are attributed, in many cases to the blocking of ion channels, such as voltage-gated calcium channels. It can also be observed that monoterpenes and monoterpenoids can have their effects modulated by the action of the vascular endothelium. In addition, it has been shown that the molecular structure and the presence of chemical groups influence the potency and efficacy of these compounds on vascular beds. Here, the effect of several monoterpenes and monoterpenoids on systemic blood pressure and vascular smooth muscle will be reported.

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Arterial smooth muscle cell PKD2 (TRPP1) channels regulate systemic blood pressure

eLife ◽

10.7554/elife.42628 ◽

2018 ◽

Vol 7 ◽

Cited By ~ 9

Author(s):

Simon Bulley ◽

Carlos Fernández-Peña ◽

Raquibul Hasan ◽

M Dennis Leo ◽

Padmapriya Muralidharan ◽

...

Keyword(s):

Blood Pressure ◽

Smooth Muscle ◽

Smooth Muscle Cell ◽

Muscle Cell ◽

Transient Receptor Potential ◽

Trp Channels ◽

Systemic Blood Pressure ◽

Trp Channel ◽

Systemic Blood ◽

Arterial Smooth Muscle

Systemic blood pressure is determined, in part, by arterial smooth muscle cells (myocytes). Several Transient Receptor Potential (TRP) channels are proposed to be expressed in arterial myocytes, but it is unclear if these proteins control physiological blood pressure and contribute to hypertension in vivo. We generated the first inducible, smooth muscle-specific knockout mice for a TRP channel, namely for PKD2 (TRPP1), to investigate arterial myocyte and blood pressure regulation by this protein. Using this model, we show that intravascular pressure and α1-adrenoceptors activate PKD2 channels in arterial myocytes of different systemic organs. PKD2 channel activation in arterial myocytes leads to an inward Na+ current, membrane depolarization and vasoconstriction. Inducible, smooth muscle cell-specific PKD2 knockout lowers both physiological blood pressure and hypertension and prevents pathological arterial remodeling during hypertension. Thus, arterial myocyte PKD2 controls systemic blood pressure and targeting this TRP channel reduces high blood pressure.

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Decision letter: Arterial smooth muscle cell PKD2 (TRPP1) channels regulate systemic blood pressure

10.7554/elife.42628.022 ◽

2018 ◽

Keyword(s):

Blood Pressure ◽

Smooth Muscle ◽

Smooth Muscle Cell ◽

Muscle Cell ◽

Systemic Blood Pressure ◽

Arterial Smooth Muscle Cell ◽

Systemic Blood ◽

Arterial Smooth Muscle

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Author response: Arterial smooth muscle cell PKD2 (TRPP1) channels regulate systemic blood pressure

10.7554/elife.42628.023 ◽

2018 ◽

Author(s):

Simon Bulley ◽

Carlos Fernández-Peña ◽

Raquibul Hasan ◽

M Dennis Leo ◽

Padmapriya Muralidharan ◽

...

Keyword(s):

Blood Pressure ◽

Smooth Muscle ◽

Smooth Muscle Cell ◽

Muscle Cell ◽

Systemic Blood Pressure ◽

Author Response ◽

Arterial Smooth Muscle Cell ◽

Systemic Blood ◽

Arterial Smooth Muscle

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The Influence of Lysine-8-vasopressin, Oxytocin, and Adrenaline on Vascular Smooth Muscle in the Human Finger

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y73-042 ◽

1973 ◽

Vol 51 (4) ◽

pp. 284-290 ◽

Cited By ~ 1

Author(s):

Peter Gaskell

Keyword(s):

Blood Pressure ◽

Smooth Muscle ◽

Vascular Resistance ◽

Young Women ◽

Systemic Blood Pressure ◽

Apparent Effect ◽

Opening Pressure ◽

Systemic Blood ◽

Critical Opening ◽

Human Finger

Lysine-8-vasopressin, oxytocin, or adrenaline was administered by intravenous infusion to young women, and their effect on the critical opening pressure (COP) of digital vessels, vascular resistance in the finger, and systemic blood pressure was measured. All doses of lysine-8-vasopressin between 0.001 and 0.08 U/min increased the COP of digital vessels but only the largest dose raised blood pressure slightly. A dose of 0.04 U/min had little if any effect on overall vascular resistance in the finger. Nevertheless the smallest dose given (0.001 U/min), which is within the physiological range of secretion rate by the pituitary gland, increased the COP of digital vessels substantially. Oxytocin at doses of 5–160 mU/min had no apparent effect on COP or vascular resistance of digital vessels or on blood pressure. Adrenaline at 4 μg/min increased the COP of digital vessels substantially. The latter observation is consistent with the absence of β receptors in vessels of the skin of the fingers.

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TRPV1 expressed throughout the arterial circulation enables inflammatory vasoconstriction

10.1101/2020.02.04.934117 ◽

2020 ◽

Author(s):

Thieu X. Phan ◽

Hoai T. Ton ◽

Hajnalka Gulyás ◽

Róbert Pórszász ◽

Attila Tóth ◽

...

Keyword(s):

Blood Pressure ◽

Skeletal Muscle ◽

Smooth Muscle ◽

Ex Vivo ◽

Systemic Blood Pressure ◽

Sensory Nerves ◽

Systemic Blood ◽

Signaling Mechanism ◽

Arterial Circulation

AbstractThe capsaicin receptor, TRPV1, is a key ion channel involved in inflammatory pain signaling. Although mainly studied in sensory nerves, there are reports of TRPV1 expression in isolated segments of the vasculature, but whether the channel localizes to vascular endothelium or smooth muscle is controversial and the distribution and functional roles of TRPV1 in arteries remain unknown. We mapped functional TRPV1 expression throughout the mouse arterial circulation. Analysis of reporter mouse lines TRPV1PLAP-nlacZ and TRPV1-Cre:tdTomato combined with Ca2+ imaging revealed specific localization of TRPV1 to smooth muscle of terminal arterioles in the heart, fat and skeletal muscle. Capsaicin evoked inward currents and raised intracellular Ca2+ levels in arterial smooth muscle cells, constricted arterioles ex vivo and in vivo and increased systemic blood pressure in mice and rats. Further, capsaicin markedly and dose-dependently reduced coronary flow. Pharmacologic and/or genetic disruption of TRPV1 abolished all these effects of capsaicin as well as vasoconstriction triggered by lysophosphatidic acid, a bioactive lipid generated by platelets and atherogenic plaques. Notably, ablation of sensory nerves did not affect the responses to capsaicin revealing a vascular smooth muscle-restricted signaling mechanism. Moreover, unlike in sensory nerves, TRPV1 function in arteries was resistant to activity-induced desensitization. Thus, TRPV1 activation in vascular myocytes of resistance arterioles enables a persistent depolarizing current, leading to constriction of coronary, skeletal muscle, and adipose arterioles and a sustained increase in systemic blood pressure.

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