NCERT grounding
NCERT Class 11 Biology, Chapter 19, Section 19.3 — Hormones of Heart, Kidney and Gastrointestinal Tract — establishes the principle that endocrine activity is not confined to the named ductless glands. Tissues whose primary roles are mechanical, filtering or digestive also contain endocrine cells that release peptide hormones into the bloodstream. The same section is summarised in the chapter recap and reappears in NIOS Biology Chapter 17 under the broader endocrine survey.
"Hormones are also secreted by some tissues which are not endocrine glands."
NCERT Class 11 · Section 19.3
This sentence is the conceptual hinge of the subtopic. Every NEET question on this section rewards a student who can map a hormone to a non-classical source and to one or two effects. The textbook does not assign a diagram to this section, so candidates often skim it; that is precisely why the matching-type items in NEET 2021, 2023 and earlier years are derived from this one page.
Non-classical endocrine sources at a glance
Three organ groups release hormones despite not being labelled as endocrine glands in NCERT: the heart, the kidney and the gastrointestinal tract. The hormones released are exclusively peptides — none are steroids, none are amine derivatives. That single chemical-class fact eliminates many distractors in NEET multiple-choice items where steroid examples are slipped in to trap unwary candidates.
Memory hook. Three tissues, six hormones, all peptides. Heart → 1 hormone (ANF). Kidney → 1 hormone (erythropoietin in NCERT 19.3). GIT → 4 hormones (gastrin, secretin, CCK, GIP).
Heart
ANF
Atrial wall · 1 hormone
Trigger: atrial stretch from rising BP.
Effect: vasodilation → ↓BP.
NEET 2016, 2023Kidney
Erythropoietin
JG cells · 1 hormone (NCERT 19.3)
Trigger: hypoxia in renal cortex.
Effect: stimulates erythropoiesis.
NEET 2021GIT
Gastrin · Secretin
CCK · GIP — 4 hormones
Triggers: meal, chyme, fat in duodenum.
Effects: control digestive secretions.
NEET 2023Heart — atrial natriuretic factor (ANF)
The atrial wall of the heart is histologically a cardiac muscle layer, yet specialised myocytes within it produce and release a peptide hormone called atrial natriuretic factor, commonly abbreviated ANF (also termed atrial natriuretic peptide, ANP, in many physiology texts). The release of ANF is mechanical in trigger: when the venous return to the right atrium and the arterial pressure rise, the atrial walls are physically stretched. Stretch-sensitive secretory granules respond by releasing ANF into the circulating blood.
The biological consequence is a fall in blood pressure. ANF acts on vascular smooth muscle to cause dilation of blood vessels, lowering peripheral resistance. It also acts on the kidney to promote sodium and water excretion — the property the name "natriuretic" describes — although NCERT itself stresses only the blood-vessel dilation pathway. The net effect is a feedback loop that opposes hypertension. Because aldosterone, secreted by the adrenal cortex, raises blood pressure by retaining sodium, NCERT treats ANF and aldosterone as physiologically antagonistic; this antagonism was directly tested in NEET 2016 in a "not antagonistic" item where the wrong pair was the answer.
Figure 1. Rising blood pressure stretches the atrial wall, triggering ANF release. ANF dilates the blood vessels and reduces blood pressure — a negative-feedback loop that opposes hypertension.
For NEET purposes, the four examinable facts about ANF are: (i) it is a peptide hormone; (ii) its source is the atrial wall of the heart; (iii) its trigger is increased blood pressure; and (iv) its effect is vasodilation and a fall in blood pressure. NCERT does not require knowledge of the molecular receptor — it is, in fact, a guanylyl-cyclase-coupled receptor producing cGMP — but the textbook does establish ANF as the canonical example of a hormone whose source is not a classical gland.
Kidney — erythropoietin and friends
The kidney is described in NCERT Section 19.3 as a hormone-producing tissue through one cell type: the juxtaglomerular (JG) cells. These modified smooth-muscle cells line the afferent arteriole at the vascular pole of the renal corpuscle. They sense plasma sodium, perfusion pressure and — relevant to this subtopic — local oxygen tension. When the renal cortex senses hypoxia, the JG cells release a peptide hormone called erythropoietin.
Erythropoietin enters the circulation and acts on the bone-marrow erythroid precursors, stimulating their proliferation and maturation into red blood cells. NCERT phrases this as "stimulates erythropoiesis (formation of RBC)." A drop in blood oxygen — caused by anaemia, high altitude or chronic lung disease — therefore triggers a hormonal correction that increases the oxygen-carrying capacity of blood over days to weeks.
Erythropoietin source
The juxtaglomerular cells of the kidney secrete erythropoietin. This was directly asked in NEET 2021 Q.151, with bone-marrow cells, pancreatic alpha cells and adenohypophysis offered as distractors.
The same JG apparatus secretes renin, which initiates the renin–angiotensin–aldosterone system (RAAS) — the classical pathway that opposes ANF and raises blood pressure when perfusion falls. NCERT covers RAAS in the excretory-system chapter; for this subtopic, students should remember that renin is also a peptide and is anatomically housed in the same JG cells, even though the textbook does not list renin under Section 19.3. The kidney additionally completes the activation of calcitriol (1,25-dihydroxy-vitamin D), the active form of vitamin D, by hydroxylating its precursor; this hormonal role is referenced in the calcium-homeostasis context rather than in 19.3.
GIT — gastrin, secretin, CCK and GIP
The endocrine cells scattered through the mucosa of the gastrointestinal tract are not collected into a discrete gland; they release four peptide hormones whose collective role is to coordinate digestion. NCERT names these four explicitly — gastrin, secretin, cholecystokinin (CCK) and gastric inhibitory peptide (GIP) — and describes them in three lines that NEET has converted into multiple matching items.
Sequential action of GIT hormones during a meal
-
Step 1
Gastrin
Released from gastric mucosa when food enters the stomach. Acts on gastric glands → secretion of HCl and pepsinogen.
Stomach -
Step 2
Secretin
Released from duodenal mucosa when acidic chyme arrives. Acts on exocrine pancreas → secretion of water and bicarbonate ions.
Duodenum -
Step 3
CCK
Released from duodenum in response to fats and partly digested proteins. Acts on pancreas (enzymes) and gall bladder (bile release).
Pancreas + gall bladder -
Step 4
GIP
Released from upper small intestine. Inhibits gastric secretion and motility; modulates digestive throughput.
Stomach (inhibits)
Each of these four hormones is a peptide, each is released in response to a chemical or physical cue from the meal, and each acts at a downstream digestive station. The clean source-target-effect mapping is what makes this section ripe for matching items: the NEET 2023 Q.184 paper aligned CCK with the pancreas, GIP with gastric glands (as the site it acts upon), and ANF with the heart — the answer key rewarded students who had memorised the source-effect pairs from this NCERT section.
Gastrin in detail
Gastrin is the cephalic-and-gastric-phase hormone. It is released by the G-cells of the gastric antrum when food distends the stomach and when peptides reach the pyloric region. NCERT compresses its physiology to one sentence: gastrin "acts on the gastric glands and stimulates the secretion of hydrochloric acid and pepsinogen." For NEET, that one sentence is the entire examinable content — students must associate gastrin with the stomach as both source and target organ.
Secretin in detail
Secretin holds a historic place in physiology: it was the first molecule to be identified as a hormone, by Bayliss and Starling in 1902. NCERT does not include this history, but the conceptual point is that secretin is released by the duodenal mucosa when acidic chyme enters from the stomach. Its target is the exocrine pancreas, where it stimulates the secretion of water and bicarbonate ions. The bicarbonate neutralises the gastric acid, raising the duodenal pH to a range at which pancreatic enzymes can act.
Cholecystokinin (CCK) in detail
Cholecystokinin has two simultaneous targets, and this two-target feature is the most asked CCK fact in NEET. The hormone acts on the pancreas, where it stimulates the secretion of pancreatic enzymes (trypsinogen, chymotrypsinogen, amylase, lipase), and it acts on the gall bladder, where it causes contraction and release of bile juice into the duodenum. The name itself encodes the gall-bladder action: chole- (bile) + cysto- (sac) + -kinin (movement).
Gastric inhibitory peptide (GIP) in detail
GIP is the only one of the four that primarily inhibits rather than stimulates. Its NCERT-listed action is to inhibit gastric secretion and motility — the upper small intestine sends GIP back to the stomach to slow its activity once chyme has been delivered. Physiology texts add that GIP also stimulates insulin release from the pancreas (an incretin effect), but this property is not part of the NCERT description and is therefore not the answer NEET expects when GIP is matched with a "primary action."
Secretin
HCO₃⁻ + H₂O
From exocrine pancreas
- Source: duodenal mucosa
- Stimulus: acidic chyme entering duodenum
- Single target: exocrine pancreas
- Effect: secretion of water and bicarbonate ions
- Net physiological role: neutralises gastric acid
Cholecystokinin (CCK)
Enzymes + bile
From pancreas + gall bladder
- Source: duodenal mucosa
- Stimulus: fats and proteins in duodenum
- Two targets: pancreas and gall bladder
- Effect: pancreatic enzymes + bile release
- Net physiological role: digests fats and proteins
Integration with digestion and circulation
The six hormones in this subtopic do not act in isolation. ANF and aldosterone form a blood-pressure pair: rising pressure releases ANF and depresses aldosterone, while falling pressure does the opposite. Erythropoietin and ANF share a tissue (the kidney is in the loop for both pressure regulation and red-cell production) but address different physiological problems — oxygen carriage versus volume control. The four GIT hormones tile the meal in sequence, with gastrin acting on the stomach, secretin and CCK on the pancreas and gall bladder, and GIP closing the loop by slowing the stomach.
NCERT closes the section with one further observation: "several other non-endocrine tissues secrete hormones called growth factors. These factors are essential for the normal growth of tissues and their repairing/regeneration." Growth factors are not given individual names in the Class 11 textbook, but the sentence is occasionally used by NEET as a distractor — a candidate must recognise that growth factors are released by non-endocrine tissues, just as ANF and erythropoietin are, and that they are not classical pituitary hormones.
Worked examples
Match each hormone with the tissue that secretes it: (a) ANF (b) Erythropoietin (c) CCK (d) Gastrin.
(a) ANF — atrial wall of the heart. (b) Erythropoietin — juxtaglomerular cells of the kidney. (c) CCK — endocrine cells of the duodenal mucosa (gastrointestinal tract). (d) Gastrin — gastric mucosa (gastrointestinal tract). The same matching pattern appears in NEET 2023 Q.184 with ANF mapped to the heart and CCK to the pancreas-and-gall-bladder action axis.
Identify the pair that is NOT antagonistic: (1) insulin–glucagon; (2) aldosterone–ANF; (3) relaxin–inhibin; (4) parathormone–calcitonin.
Insulin–glucagon work opposite ways on blood glucose; aldosterone raises BP while ANF lowers it; parathormone raises blood calcium while calcitonin lowers it. Relaxin and inhibin both belong to the reproductive cluster but do not act in opposite directions on the same parameter, so option (3) is the correct "not antagonistic" pair. NEET 2016 Q.83 used this exact frame.
A patient with chronic kidney disease becomes severely anaemic. Which hormone is most likely deficient, and why?
Erythropoietin. The juxtaglomerular cells of the kidney secrete erythropoietin, which stimulates erythropoiesis in the bone marrow. When renal tissue is damaged, erythropoietin output falls, red-cell production is no longer adequately stimulated, and the patient develops the anaemia of chronic kidney disease.