The physiology, pharmacology, and biochemistry of the eccrine sweat gland

The sections in this article are:


1
Basal Vascular Resistance and Autoregulation

2
Role of Myogenic Mechanism in Reactive Hyperemia

3
Role of Myogenic Mechanism in Exercise Hyperemia

4
Types of Skeletal Muscle Fibers

5
Muscle Blood Flow During Exercise
5.1
Oxygen Lack

5.2
Lactic Acid, pH, and CO2

5.3
Potassium

5.4
Inorganic Phosphate

5.5
Osmolarity

5.6
Prostaglandins

5.7
Adenosine and Adenine Nucleotides

5.8
Intrinsic Neurons and Exercise Dilatation

5.9
General Conclusions




6
Mechanical Hindrance to Blood Flow in Skeletal Muscle

7
Reactive Hyperemia
7.1
Are Exercise and Reactive Hyperemia Due to the Same Mechanism(s)?




8
Propagated Vasodilatation

9
Sympathetic Vasomotor Outflow

10
Noradrenergic Innervation of Resistance Vessels in Muscles
10.1
Neuroeffector Junction

10.2
α-Adrenergic Activation




11
Factors that Modulate Transmitter Output From Sympathetic Nerve Endings
11.1
Metabolic Action

11.2
Neurohumoral Action




12
Reflex Regulation of Skeletal Muscle Resistance Vessels by Sympathetic Noradrenergic Nerves
12.1
Carotid and Aortic Baroreflex

12.2
Carotid and Aortic Chemoreflex

12.3
Reflexes From the Heart and Lungs

12.4
Diving Reflex

12.5
Reflex From Receptors in Skeletal Muscles




13
Rhythmic Exercise

14
Isometric Exercise

15
Influence of Sympathetic Noradrenergic Fibers on the Blood Flow to Active Muscles

16
β2-Adrenergic Activation

17
Cholinergic Vasodilator Nerves
17.1
Role of Cholinergic Nerves in the Carotid Baroreflex

17.2
Cholinergic Vasodilatation in Humans




18
Histaminergic Vasodilatation
18.1
Role of Histamine in the Vasodilatation Resulting From Reflex Inhibition of Sympathetic Outflow




19
Conclusions

Circulation to Skeletal Muscle

SummaryIn unanesthetized dogs abdominal aortic pressure was measured with an implanted miniature transducer, left renal artery flow velocity by an electromagnetic flowmeter.The effect of rapid injections (<1 sec) of 2.5, 5.0, 10.0 and 20.0 μg isoproterenol into the abdominal aorta proximal to the renal artery on kidney blood flow and arterial blood pressure was investigated.Isoproterenol in every dose used regularly caused kidney blood flow to increase and arterial blood pressure to fall. The maximum decrease of resistance to flow in the average amounted to 25–30%. During the first 6 sec after drug injection kidney blood flow was already significantly elevated while arterial blood pressure was still unchanged.A significantly augmented kidney blood flow was also found when blood pressure had returned again to its original level.After β-blockade (0,5 mg/kg propranolol) isoproterenol (2.5–20.0 μg i.a.) had no effect on kidney blood flow and arterial blood pressure.The extent of the vasodilation cannot be attributed to autoregulation. It is concluded, that isoproterenol (2.5–20.0 μg i.a.) causes a β-adrenergic vasodilation in the kidney vasculature of the resting conscious dog.ZusammenfassungAn wachen Hunden wurden mit einem Miniaturdruckaufnehmer der Blutdruck in der abdominalen Aorta und mit einem elektromagnetischen Flußmesser die Strömungsgeschwindigkeit in der linken Nierenarterie gemessen.Die Reaktion der Nierenstromstärke und des Blutdrucks auf rasche (<1 sec) Injektion von 2,5, 5,0, 10,0 und 20,0 μg Isoproterenol in die abdominale Aorta proximal der Nierenarterie wurde untersucht.Bei allen vier Dosen wurde regelmäßig eine Steigerung der Nierendurchblutung und eine Abnahme des arteriellen Blutdrucks beobachtet. Die maximale Widerstandssenkung betrug im Mittel 25–30%. Während der ersten 6 sec nach Injektion erreichte die Nierenstromstärke bei noch unverändertem arteriellen Mitteldruck einen signifikant erhöhten Wert. Ebenso fand sich eine signifikant erhöhte Stromstärke, nachdem der Blutdruck sein Ausgangsniveau wieder erreicht hatte.Nach β-Blockade mit 0,5 mg/kg Propranolol hatte Isoproterenol in den verwendeten Dosen keinen Einfluß auf die Nierenstromstärke und den arteriellen Blutdruck.Das Ausmaß der beobachteten Vasodilatation läßt sich durch Autoregulation nicht erklären. Aus den Experimenten wird geschlossen, daß Isoproterenol (2,5 bis 20,0 μg i.a.) am wachen Hund in Ruhe β-Receptoren der Nierengefäße erregt.

Demonstration of a beta adrenergic dilatation of renal vessels in the awake dog

For a long time the role of renal nerves in the regulation of renal function was considered to be of low importance. Smith stated in 1951: “Renal denervation in unanaesthetized normal dogs and men does not produce renal hyperemia, the vasoconstrictor pathways being quiescent under basal conditions; nor does renal denervation have any significant effect upon the normal urine flow, upon water diuresis, or pituitary antidiuresis.” The demonstration of rich sympathetic innervation of the juxtaglomerular apparatus and tubular epithelium (for review see Barajas, 1978) is the basis for the action of the nervous system and catecholamines on the kidney. Electrical stimulation of the renal nerves was found by Vander (1965) to increase renal venous renin activity. It was only recently that a direct effect of renal nerve stimulation on tubular electrolyte reabsorption was clearly demonstrated by Di Bona (1977). Thus, there is morphological and functional evidence that renal sympathetic nerves are intimately involved in the regulation of the secretory and excretory function of the kidney.

Effects of Adrenergic Activators and Inhibitors on Kidney Function

The thermogenic action of beta-adrenoceptor agonists may be due, in part, to increased metabolism in skeletal muscle. Previous results suggest that vasoconstriction is also necessary, and that the effect can be blocked by vasodilators. Both noradrenaline and the beta-3 agonist, ICI D7114, were studied using two dog hindlimb protocols. During constant perfusion conditions, ICI D7114 caused a significant increase in hindlimb oxygen consumption although it is a vasodilator. Noradrenaline resulted in a smaller rise in oxygen consumption, and produced a marked vasoconstriction. Both noradrenaline and ICI D7114 resulted in decreased oxygen consumption when the blood flow was allowed to vary in response to the drug treatment. The results suggest that changes in tissue oxygen consumption caused by beta-agonists are not related to vasomotion.

The effects of thermogenic agents on hindlimb oxygen consumption in the dog: ICI D7114 and noradrenaline.

The effects of blockade and stimulation of beta adrenergic receptors on mesenteric, renal and hindlimb circulations have been investigated in unanesthetized resting dogs. Propranolol and isoproterenol have been used for beta blockade and stimulation, respectively. The changes in oxygen consumption in the hindlimb following beta receptor stimulation have also been studied in some experiments performed under anesthesia.

Beta adrenergic receptor activity in peripheral vascular beds of the unanesthetized dog.

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Beta adrenergic receptor activity in peripheral vascular beds of the unanesthetized dog.