Carbohydrate Metabolism and Stress: The Roles of Glucagon and Insulin
Stress and prolonged physical exertion require the immediate mobilization of energy reserves. This task is performed by glucagon, a hormone secreted by $\alpha$-cells of the pancreatic islets (islets of Langerhans) that acts as the primary antagonist of insulin.
Glucagon secretion is stimulated by hypoglycemia, stress, physical exercise, and the sympathetic nervous system, as well as by growth hormone (via somatomedins). Its production is inhibited by insulin, somatostatin, and high glucose levels.
Physiological effects of glucagon:
- Carbohydrate metabolism: Exerts a pronounced hyperglycemic effect. It activates glycogen phosphorylase (stimulating glycogenolysis) and inhibits glycogen synthase (suppressing glycogenesis). Gluconeogenesis is additionally stimulated.
- Lipid metabolism: Exerts lipolytic and ketogenic effects. Triglyceride levels decrease, and ketone bodies appear in the blood.
- Outcome: Tissues receive the glucose and ketone bodies necessary to overcome stress.
Insulin secretion is similarly regulated: parasympathetic stimulation enhances it, whereas sympathetic influence and the paracrine action of somatostatin (from $\delta$-cells) inhibit it. Somatostatin acts by activating an inhibitory G-protein cAMP system, suppressing the secretion of numerous cells, including insulin and glucagon.
Adaptation to Circadian Rhythms: The Pineal Gland and Melatonin
The pineal gland is a neuroglial-derived gland that synthesizes biogenic amines (serotonin, norepinephrine, histamine) and peptide hormones. The primary factor in adapting to changing lighting conditions is melatonin.
Melatonin synthesis depends directly on illumination: signals are perceived by the retina and transmitted reflexively via the sympathetic nervous system. In the light, the conversion of serotonin to melatonin is inhibited, whereas in the dark, it is sharply accelerated. This cyclical production determines circadian biological rhythms.
Effects of melatonin:
- Sleep regulation: Elevated hormone levels produce a sedative effect, facilitating the transition from wakefulness to sleep.
- Metabolism suppression: Inhibits the secretion of metabolism-enhancing hormones (ACTH, TSH, GH).
- Reproductive influence: Determines the cyclicity of gonadotropic effects (including the duration of the ovarian-menstrual cycle).
Mineral Metabolism Adaptation: The Parathyroid Glands
Two pairs of parathyroid glands, located posterior to or embedded within the thyroid gland, secrete parathyroid hormone (PTH). Its sole objective is to maintain normal blood calcium levels via strict negative feedback: a drop in calcium stimulates PTH production, while an increase inhibits it.
Mechanisms of PTH action:
- In bone tissue: Activates osteoclasts, causing bone demineralization and the release of calcium into the blood.
- In the kidneys: Enhances calcium reabsorption, decreases phosphate reabsorption (increasing phosphate excretion), and stimulates the synthesis of calcitriol, the active form of vitamin D.
Hemodynamic Adaptation: The Endocrine Role of the Kidneys and the RAAS
Although the kidneys lack specialized endocrine glands, their cells produce numerous biologically active substances: calcitriol, erythropoietin, thrombopoietin, prostaglandins, and kallikrein. A prominent role is played by renin, an enzyme produced by the juxtaglomerular apparatus that initiates the renin-angiotensin-aldosterone system (RAAS).
Factors activating renin secretion:
- A drop in blood pressure within the afferent arteriole.
- Elevated $Na^+$ ion concentration in the distal tubule fluid (detected by the macula densa).
- Sympathetic inputs (via $\beta$-adrenergic receptors) and adrenaline.
Note: Atrial natriuretic peptide and high blood pressure inhibit renin secretion.
The RAAS cascade and its effects:
- Renin converts circulating plasma angiotensinogen (synthesized in the liver) into the weakly active angiotensin I.
- Angiotensin-converting enzyme (ACE, predominantly pulmonary) converts it into active angiotensin II.
Angiotensin II causes powerful vasoconstriction, activates the sympathetic nervous system, triggers thirst, and stimulates the zona glomerulosa of the adrenal cortex to secrete aldosterone. Aldosterone, in turn, increases the reabsorption of $Na^+$, $Cl^-$, and $HCO_3^-$ in the kidneys, leading to water retention. The system is regulated by negative feedback depending on blood levels of $Na^+$, $K^+$, angiotensin, and aldosterone.